FAR EASTERN UNIVERSITY

Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Endocrine-Metabolism

Module 1 Care of Clients with GI and Metabolism Disorders

Review of Anatomy, Physiology, and Functions of the GI System

Outline 4. Elimination – is the removal of undigested

1. Review of Anatomy, Physiology, and material, such as fiber from food, plus other
Functions of the GI System waste products from the body as feces.
2. Assessment and Diagnostic Procedures Organs of the Digestive System:
3. Disturbances in GIT-Metabolism 1. Alimentary Canal Organs
a. Disturbances in Ingestion Also called the gastrointestinal (GI) tract or
b. Disturbances in Digestion gut, the alimentary canal (aliment- = “to
c. Disturbances in Absorption and nourish”) is a one-way tube about 7.62 meters
Elimination (25 feet) in length during life and closer to
10.67 meters (35 feet) in length when
Review of Anatomy, Physiology and Functions of measured after death, once smooth muscle
the Gastro Intestinal System tone is lost. The main function of the organs
of the alimentary canal is to nourish the body.
The Gastrointestinal System is a 23- to 26 foot This tube begins at the mouth and terminates
pathway for food, water, vitamins and minerals for at the anus. Between those two points, the
which has the primary function of breaking down canal is modified as the pharynx,
food products that can fuel the body as a source of esophagus, stomach, and small and large
energy intestines to fit the functional needs of the
body. Both the mouth and anus are open to
All cells of the body require nutrients. These the external environment; thus, food and
nutrients are derived from the intake of food wastes within the alimentary canal are
that contains proteins, fats, carbohydrates, vitamins technically considered to be outside the body.
and minerals, and cellulose fibers and other Only through the process of absorption do the
vegetable matter of no nutritional value. nutrients in food enter into and nourish the
The primary digestive functions of the GI tract are body’s “inner space.”
the following:
1. Ingestion – is the consumption of solid or 2. Accessory Organs /Structures
liquid food, usually through the mouth. Within the mouth, the teeth and
2. Digestion – is the breakdown of large tongue begin mechanical digestion, whereas
organic molecules into smaller molecules the salivary glands begin chemical digestion.
that can be absorbed. Digestion occurs Once food products enter the small intestine,
through mechanical and chemical means. the gallbladder, liver, and pancreas release
3. Absorption – is the movement of molecules secretions—such as bile and enzymes—
out of the digestive tract and into the blood or essential for digestion to continue. Together,
the lymphatic system. The epithelial cells that these are called accessory organs because
line the lumen of the small intestine absorbs they sprout from the lining cells of the
the small molecules of nutrients (amino developing gut (mucosa) and augment its
acids, monosaccharaides, fatty acids, function; indeed, you could not live without
vitamins, minerals and water) that result from their vital contributions, and many significant
the digestive process. diseases result from their malfunction. Even
 after development is complete, they maintain called chyme. Gastric secretions and
a connection to the gut by way of ducts. motility is governed by hormones,
neuroregulators, and local regulators.
Digestive System Processes and Regulation
The digestive system uses mechanical and chemical 5. Small Intestines
activities to break food down into absorbable Upon reaching the duodenum, accessory organs
substances during its journey through the digestive contribute to the secretions encountered by food
system. therein:
1. Process of Chewing or Mastication • Pancreas: secretes alkaline pH, high in
• The salivation reflex is stimulated just by concentrations of bicarbonate, to
the sight, smell, or tasting food. About 1.5 neutralize the acid entering the duodenum
liters of saliva is secreted daily by the 3 from the stomach. Digestive enzymes
pairs of glands – parotid, submaxillary, involved from the pancreas are:
and sublingual glands. 1. Trypsin: digests proteins.
• Saliva contains the enzyme ptyalin, or 2. Amylase: digests starch.
salivary amylase, which begins the 3. Lipase: digests fats.
digestion of starches. 1. Liver: secretes bile which emulsifies fats.

2. Swallowing 2. Gallbladder: stores bile secreted by the liver

Upon swallowing, the epiglottis moves to cover that will aid in the digestion and absorption
the tracheal opening and prevent swallowing. of fats.
o Small, fingerlike projections called
3. Esophageal Peristalsis villi are present in the entire intestines
A reflex action into the upper esophagus propels that produce the digestive enzymes
the bolus of food contracting in a rhythmic and absorb nutrients from food.
sequence toward the stomach. The process of Absorption is the primary function of
esophageal peristalsis simultaneously relaxes the the small intestines which begins in
esophageal sphincter to permit this movement of the jejunum by active transport and
food to the stomach. diffusion across the intestinal wall.
6. Large Intestines
4. Stomach • After four hours of eating, waste residuals
The stomach produces acidic fluid called the are passed in the terminal ileum into the
hydrochloric acid. Its purpose is to further proximal portion of the colon through the
breakdown food into a more absorbable ileocecal valve. Bacteria make up a major
component and to aid in the destruction of component of its contents which are
ingested bacteria. neutralized by electrolyte secretions and
• The enzyme pepsin, initiates protein mucus. Controlled by the autonomic
digestion. nervous system (parasympathetic nerve
• Intrinsic factor is also secreted by the gastric fibers as a spinal reflex), defecation is
mucosa which combines with dietary vitamin elicited by the relaxation of the external
B12 so that it can be absorbed in the ileum. anal sphincter.
The absence of this intrinsic factor results to
pernicious anemia.
• Peristalsis in the Stomach
o Peristalsis in the stomach (about half
hour to several hours) propels food to
the pylorus. The pyloric sphincter
contracts to allow food to move
towards the small intestines. Food
mixed with gastric secretions is
 FAR EASTERN UNIVERSITY
Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Endocrine-Metabolism

Assessment and Diagnostic Procedures of the Gastrointestinal System

Health History • Barium Sulfate (BaSO4) per orem

• Demographic Data (age, sex) • X – rays taken on standing, lying position
• Personal & Family History • After the procedure
• Diet History • Laxative
• Chief Complaint o Increase fluid intake
– Onset o Inform client that the stool is
– Duration white for 24 – 72 hours
– Quality & Severity o Observe for Barium impaction :
– Location distended abdomen constipation
• Precipitating Factors
• Relieving Measures 3. LGIS ( Barium Enema)
• Associated Symptoms
• Family History
• Psychosocial History

Physical Examination/Review of Systems

• Inspection
• Palpation
• Percussion
• Auscultation

Diagnostic Procedures
• To visualize the colon
Non-invasive • Low residue / clear liquid diet for 2 days
Radiological Studies
• Laxative for cleansing the bowel
1. Scout Film/Flat Plate of the Abdomen
• Suppository / cleansing enema in A.M.
• Plain X – ray of the abdomen
• BaSO4 per rectum
• Recumbent Position, belts / jewelries
• Care after the procedure – same as UGIS
2. UGIS (Barium S wallow)
4. Ultrasound
• NPO for 8-12 hours
• Laxative as ordered (bowel gas)

5. Magnetic Resonance Imaging

• produces cross sectional images of soft
tissues and blood vessels using magnetic
fields.
• C/I: pacemakers, aneurysm clips, or
• To visualize the esophagus, stomach, orthopedic screws
duodenum and jejunum • NPO 6h before
• NPO for 6 – 8 hours • Instruct to lie still for 60-90 mins.
 • Remove all Metals (jewelry, dentures,
eyeglasses)

6. CT Scan

2. LGI Endoscopy
• produces cross sectional images of a. Proctosigmoidoscopy (sigmoid,
internal organs, bones, soft tissue and rectum)
blood vessels • Obtain written consent
• with or without contrast • Clear liquid diet 24 hours before
• C/I: Allergy to shellfish; pregnancy • Administer cathartic / laxative as
• NPO 4-6 hrs. ordered
• Remove all Metals (jewelry, dentures, • Cleansing enema
eyeglasses) • Knee – chest / lateral position
• After the procedure
7. HIDA (hepatobiliary iminodiacetic acid o Supine position for few
scan) Scan minutes
• tracks the flow of bile from the liver, o Assess for signs of
gall bladder and bile ducts perforation
• Uses radioactive tracers o Bleeding, Pain, and Fever
• C/I: Allergy to shellfish; pregnancy; o Hot sitz bath for
barium or bismuth (4 days) discomfort
• NPO 4-12 hrs

Invasive: Endoscopy b. Colonoscopy

1. UGI Endoscopy • Obtain written consent
• Direct visualization of esophagus, • Clear liquid diet 24 hours before
stomach, and duodenum • Sedation
• Obtain written consent • Position : left side, knees flexed
• NPO for 6 – 8 hours • After the procedure
• Anticholinergic (AtSO4) as ordered o Supine position for few
• Sedatives, narcotics, tranquilizers minutes
E.g. Diazepam, Meperidine HCl o Assess for signs of
• Types: perforation
o Esophagogastric o Bleeding, Pain, and Fever
duodenoscopy o Hot sitz bath for
o Capsule Endoscopy discomfort
o Double Balloon Endoscopy
 Laboratory Tests
1. D-Xylose absorption test
• Tests how well the intestines absorb a
simple sugar (D-xylose)
• 8 ounces of water that contains 25 grams
of D-xylose

2. Enzyme
Normal Low Levels High Levels
Values
Serum 40-140 Pancreatic Intestinal
amylase U/L cancer obstruction
damage to Infection of
pancreas salivary glands
Liver Perforated ulcer
disease cholecystitis
Serum 0-160 Chronic Gastroenteritis
lipase U/L pancreatitis Pancreatic
Liver cancer
disease Pancreatitis
Cholecystitis

3. Liver Function Test

3. Other Endoscopic Procedures Normal Low levels High levels
values
a. Endoscopic Retrograde Total 6.5-8.2 Severe Chronic
Cholangiopancreatography protein g/dl malnutrition inflammation
(ERCP) Celiac infections
disease
• Visualization of common bile IBS
duct C/I: Allergy to shellfish Albumin 3.9-5-0 Cirrhosis Dehydration
• Obtain written consent g/dl Malnutrition
Inflammatio
• Clear liquid diet 24 hours before n
• Sedation Shock
Globulin 2.5-3.5 Genetic Multiple
• Position: left side during insertion g/dl deficiencies myeloma
(Leukemia) Autoimmune
Invasive: Other GI Tests diseases
A/G >1 Autoimmun Genetic
1. Bernstein test (Acid perfusion test) ratio e disease deficiencies
• reproduce symptoms of heartburn Cirrhosis (Leukemia)
• Mild HCl followed by saline solution
through NGT 4. Liver Function Test (liver panel)
• NPO for 8 hours Normal Values High Levels
Alkaline 30-115 IU/L Hepatitis
• Obtain written consent phosphatase Liver cancer
Obstruction of
2. Endoscopic Ultrasound bile ducts
SGPT (ALT 5-60 IU/L Obstruction of
3. Peritoneoscopy (Diagnostic Laparoscopy) Alanine bile ducts
• measure the pressure inside the lower Transaminase) Hepatitis
part of the esophagus Liver cancer
SGOT (AST 5-43 IU/L Liver tumors
• Dx of swallowing problems Aspartate
4. Esophageal Manometry transaminase)
5. Ambulatory Esophageal pH monitoring- Bilirubin Blockage of bile
Total bilirubin 0.20-1.50 mg/dl ducts
measures how often and for how long Direct bilirubin 0.00-0.03 mg/dl Liver disease
stomach acid enters the esophagus Hemolysis
6. Exfoliative Cytology- detects malignant 5. Fecal Analysis
cells a. Fecal occult blood test (FOBT)
 • Guaiac, Hemoccult
• Detect G.I. Bleeding
• Fiber diet 48 – 72 hours
• No red meats, poultry, fish,
turnips, horseradish, coffee
b. Ova and Parasite
c. Stool Culture
d. Qualitative Fecal Fat Studies- to
assess steatorrhea
6. Gastric analysis- evaluates gastric function
by measuring acidity, appearance, and
volume
a. Gastric analysis cycle
• Basal secretion is collected every 15
minutes for 4 hours
• intramuscular administration of a drug
that stimulates gastric acid output
(betazole)
• stomach secretions is collected every 15
minutes for 90 minutes

Analysis/ Nursing Diagnosis

1. Imbalanced Nutrition: Less than Body
Requirements as evidenced by decreased
food intake, weight loss 20% or more of ideal
body weight, dry and brittle hair, weakness,
impaired tissue healing.
2. Deficient Fluid Volume as evidenced by dry
mucus membranes, poor skin turgor, thirst,
increased body temperature
3. Nausea as evidenced by complaints of
stomach discomfort, increased salivation,
tachycardia, and cold and clammy skin
4. Impaired Skin Integrity as evidenced by
disruption of skin surface, pain, itching
5. Acute Pain (Cognitive-Perceptual)
 Catchemail
FAR EASTERN UNIVERSITY
Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Endocrine-Metabolism

Disorders in GIT-Metabolism: Disturbances in Ingestion

Disorders of the Esophagus • Symptoms often are worse when lying

1. GERD flat, straining, bending at the waist or
2. Hiatal Gernia sleeping.
-

3. Diverticulosis
-

Diagnosis
4. Other Esophageal Conditions • Barium swallow
• Ambulatory Esophageal pH monitoring
Gastroesophageal Reflux Disease (GERD) • Endoscopy (EGD)
• the backflow of gastric juices into the • x-ray
esophagus, mouth and lungs 4 hydrochloric acid • Esophageal manometry
Etiology: Complications
1. Incompetent lower esophageal sphincter a. Esophageal strictures
(LES) b. Ulcers
=> Lumiit and but as

2. Transient LES relaxation c. Diverticulitis

3. Increased intragastric pressure
- d. Barrette's Esophagus
naprpush
nguten
stomach e. Esophageal
- cancer worst
Contributing factors: ung f. Esophageal Strictures- severe scarring and
• obesity narrowing of the esophagus =>
ten denayOFgoteve
• pregnancy g. Diverticulosis- outpouching of the walls of
• caffeine => Butas-butas/scarring
the esophagus > Cancer

• chocolate
-

h. Barrette’s Esophagus- replacement of the

-

• high fatty food ingestion cells lining the esophagus with cells more
• Smoking typical of the stomach or intestines
• ETOH alcohol
=
(metaplasia); occurs in approx & 10% of
• Hiatal Hernia Luslos
= patients with GERD.
• caused by long-term damage caused -

Assessment signs & Symptoms by GERD and acid

-

a. Heartburn • Precancerous condition associated

-

b. Dysphagia with cancer of the esophagus

c. back pain/ Chest pain veins
varises
d. coughing spells Planning: Nursing Diagnoses sesophageal
-

e. Hoarseness/ sore throat a. Acute pain related to tissue trauma

f. vomiting b. Imbalanced nutrition, less than body
g. Belching panay and pagburp
:
requirement related to malabsorption
• Symptoms typically occur after eating a c. Deficient Fluid Volume related to vomiting
meal d. Impaired tissue integrity related to surgery
• can be especially noticeable with a large e. Risk for infection related to surgery
meal or spicy foods.
• Symptoms may be relieved by antacids. Management
Lifestyle changes
• diet changes maintain normal weight
-
 • low fat, low cholesterol § possible complications
• Avoid tight clothing/ belts § NGT/ chest tube
• b. Consent
-

Avoid bending
• stop smoking c. NPO post-midnight
• Refrain eating 3 hrs. before bed time d. Post-op care
•
-

stay upright 2 hours after a meal a. Reinforce pre-op care

-
b. Pain management
Pharmacological > decreasi duction c. Semi-fowler’s position
d. NGT care
-

a. H2 receptor antagonist (Cimetidine,

Ranitidine, famotidine, nizatidine)- decrease e. Diet
acid production acid
f. Assess for complication
Block/stop
>
-

b. Proton Pump inhibitors (Prilosec, Prevacid, e. Administer medications

Protonix)- blocks acid production f. Referral
c. Prokinetic medications (Cisapride,
Metaclopromide)- enhances gastrointestinal Hiatal Hernia
motility • Protrusion of the stomach upward into the
d. Antacids (Maalox, Kremil S)- neutralizes mediastinal cavity through the esophageal
hiatus of the diaphragm
-

stomach acidity magnesium-diar

<

> Aluminum-consti

Surgical Types
Fundoplication- wrapping the fundus of the 1. Sliding (90% of cases)
stomach around the lower esophagus and suture the • part of the stomach moves up through
an opening (hiatus) in the diaphragm.
-

fundus to itself.
• Open Fundoplication • increases the risk for GERD
o The Nissen Fundoplication– a
complete (360°) wrap of the stomach 2. Rolling (Paraesophageal) tendency people alrespi problem
>
-

For

• The fundus and possibly portions of

-

around the esophagus Open

Fundoplication the stomach’s greater curvature, rolls
o The Toupet Fundoplication– an through the esophageal hiatus and
incomplete (270°) wrap of the into the thorax beside the esophagus
stomach around the esophagus
Complications ocaparoscopic Fundoplication Sliding Hiatal Hernia
a. Bleeding Etiology
b. Infection • Increased intra-abdominal pressure
c. Respiratory complications • Weakening of muscles in diaphragm
d. Gas Bloat syndrome inability to eructate • Age
=>palagi mayKabag/burp
(bloating, borborygmi)- avoid gas-producing
food - ambulation Contributing Factors
• Obesity
-

Nursing responsibilities • Pregnancy weakening diapraghm

mosde of

a. Assessment • Bending
a. admission assessment • Frequent hard coughing/ sneezing
b. shift & focused assessment • Weight lifting
b. Prepare client for procedure • Straining
c. Prepare client for surgery • Stress
a. Pre-op teaching
§ deep breathing & coughing Assessment
§ incentive spirometry • Heartburn
§ ambulation • Regurgitation
 • Dysphagia Pharmacological
• Belching • H2 receptor antagonist (Cimetidine,
Ranitidine, famotidine, nizatidine)
Signs and Symptoms • Proton Pump inhibitors (Prilosec, Prevacid)
• Feeling of-fullness and breathlessness after • Prokinetic medications (Cisapride,
eating Metaclopromide)
• Feeling of-
suffocation • Antacids (Maalox, Kremil S)
• Chest pain/-
back pain
Surgical
*Symptoms worse in recumbent position a. Fundoplication- wrapping the fundus of the
stomach around the lower esophagus and
-

* No reflux symptoms
suture the fundus to itself.
-

Complications b. Hill Operation- narrowing of the esophageal

• Hemorrhage/ Anemia opening and anchoring of the stomach and
• Pulmonary Aspiration the esophagus in place
• GERD - May reinforce with
• Esophagitis fundoplication
• Stenosis c. Angelchik prosthesis- C-shaped silicone
• Ulcerations of herniated portion prosthesis is tied around the distal esophagus
and anchors the LES in the abdomen
• Strangulation of hernia
Nursing Responsibilities
Diagnosis
1. Assessment
• Barium swallow a. admission assessment
• Endoscopy (EGD) b. shift & focused assessment
• CXR 2. Prepare client for the procedure.
• CBC anemia
-

3. Prepare client for surgery

• Guaiac stool -
exam
a. Pre-op teaching
- deep breathing & coughing
Planning: Nursing Diagnoses - incentive spirometry
• Acute pain related to tissue trauma - ambulation
• Imbalanced nutrition, less than body - possible complications
requirement related to dysphagia - NGT/ chest tube
• Impaired tissue perfusion related to bleeding/ b. Consent
low RBC count c. NPO post-midnight
• Impaired tissue integrity related to trauma/ 4. Post-op care
herniation a. Reinforce pre-op care
• Activity intolerance related to anemia b. Pain management
• Disturbed sleep pattern c. Semi-fowler’s position
d. NGT care
Management e. Diet
Lifestyle changes f. Assess for complication
• diet changes: maintain normal weight, low 5. Administer medications
fat, low cholesterol 6. Referral
• Avoid tight clothing/ belts
• Avoid bending Diverticulosis
• Refrain eating 3 hrs. before bed time Diverticulum- the sac-like outpouching in one or
more layers of the
• Stay upright 2 hours after a meal
esophagus
 Pharmacologic
Types: 1. Botulinum toxin injected into the LES to
1. Zenker’s Diverticulum- above the UES (most reduce resting pressure
common)
2. Midesophageal (rare) Surgical
3. Epiphrenic Diverticulum- above the LE 1. Diverticulectomy- excision of the
diverticulum and the esophageal mucosa is
Etiology: reanastomosed
1. Esophageal weakness
2. Pulsion- pushing from inside
-
Nursing responsibilities
3. Traction- pulling from outside 1. Assessment
a. admission assessment
-

Contributing Factors: b. shift & focused assessment

• Congenital 2. Prepare client for procedure
• Esophageal trauma 3. Prepare client for surgery
• Scar Tissue a. Pre-op teaching
• Chronic Inflammation § deep breathing & coughing
• Achalasia § incentive spirometry
§ ambulation
Assessment: § possible complications
• Dysphagia § NGT/ chest tube
• Aspiration b. Consent
c. NPO post-midnight
• Regurgitation*
4. Post-op care
• Halitosis a. Reinforce pre-op care
• Coughing b. Pain management
* Usually when recumbent c. Semi-fowler’s position
d. NGT care
Diagnosis e. Diet
• Barium swallow f. Assess for complication
• Esophageal manometry 5. Administer medications
• CXR 6. Referral
• Endoscopy is usually contraindicated
I

*Flexible UGI endoscopy Other Esophageal Conditions

1. Esophageal Varices- esophagEsophageal
>
-
vessus inwiravices
Planning: Nursing Diagnoses Blood
submucosal venous channel become dilated
• Imbalanced nutrition, less than body
-
secondary to portal hypertension; rupture
requirement related to dysphagia may cause exsanguination + Blood
Thydrochloric acid

• Fluid volume deficit related to dysphagia 2. Achalasia- constant contraction of the LES
• -Risk for aspiration & uncoordinated muscle contraction
•- Impaired tissue integrity related to trauma a. Dilation of the esophagus
• Disturbed sleep pattern b. Dysphagia
c. Retention of food bolus
Management: -
3. Esophageal Stenosis- narrowing of the
L
Lifestyle Changes 7 esophagus which causes obstruction
1. Diet management(semi-soft) a. Intermittent Dysphagia
2. Stay upright 2 hours after a meal b. Dysphagia for solids- pain when
3. Sleeping with HOB elevated swallowing
4. c. Retention of food bolus
·

FAR EASTERN UNIVERSITY

Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Endocrine-Metabolism

Disorders in GIT-Metabolism: Disturbances in Digestion

Disturbances in Digestion Etiology

1. General GI Symptoms Normal
2. Peptic Ulcer Disease –- Increased Attack Hyperacidity
-

3. Gastritis – Weak defense

4. Food Poisoning *Helicobacter pylori causative agent
>
-

*Stress, drugs, smoking

-

General GI Symptoms -

1. Pain maraming nerve endings and stomach Predisposing Factors

• Most characteristic a. Irregular, hurried meals (stressful)
-
• Caused by nerve irritation b. Fatty, spicy, highly acidic foods, (stimulants,
• Caused by increased motility irritants)
2. Anorexia c. Type A personality- “stress personality”
-
-

• Common with malignancies competitive (may timeframe)

• Caused by nerve irritation Predisposing Factors -

• Caused by increased motility a. -Type O blood: ­pepsinogen levelsàPEPSIN

3. Nausea and Vomiting excitation of neve impulses b. Genetics: ­ in parietal cell mass à acid
-
-

• Stimulation of chemoreceptors secretion

• Gastric stasis c. Drugs: Aspirin, anti-inflammatory (NSAIDs)
-
-

4. Bleeding & Corticosteroids always in

In stoduodestos to my full meal
⑤ Diarrhea-increase peristalsis
• Caused by trauma ③ Indigestion before taking

Complications
• Ulcers= 80% & Flatulenal & Belching
a. HEMORRHAGE : most life threatening
5. Indigestion
complication of PUD à hypovolemic shock
6. Flatulence and Belching
b. Fibrosis, Stricture obstruction – pyloric
stenosis
Peptic Ulcer Disease
c. Perforation – Peritonitis- emergency
• sore that forms in the lining of the stomach d. Gastric carcinoma Gastric Modenal
or of the duodenum Iscar-wound)
Bleed > ground
coffee
-

meleu
check fat
a

intoo Diagnosis
Types a. Endoscopy
1. Gastric
b. Barium swallow >
-lesion
see

2. Duodenal c. Biopsy – bacteria & malignancy

d. H.Pylori:
Theory – Endoscopic cytology
– Biopsy
– Special stains
– Culture – difficult
– Urea Breath test (UBT)
– ELISA – to detect antibody

Management
Medical
a. Diet modification
 –- High fiber •
– Increase fluid intake
%
Billroth I (Gastroduodenostomy)
removal of the lower portion of the
b. Prevent complications stomach and duodenum with
c. Treat complications anastomosis of the remaining portion
of the duodenum
Pharmacologic • Billroth II (Gastrojejunostomy)
- >
- masmalalim

a. Most popular treatment (second choice) - removal of the antrum and distal
– A proton pump inhibitor portion of the stomach and
– Amoxicillin treatment plus duodenum with anastomosis of the
Clarithromycin BID for10-14 days remaining portion of the stomach
b. Most popular treatment (second choice) to the jejunum
– Bismuth subsalicylate + Tetracycline gin1 - The duodenum is bypassed to
> tablet
- -

+Metronidazole QID for 10-14days permit the flow of the bile

– A proton pump inhibitor
-

d. Photocoagulation laser (for gastric

c. Other symptoms bleeding) > Laser
-
para grmaling
vicer

– Antacids - Endoscopic procedure

– H2 blockers - Can be achieved by use of the laser
• Cimetidine, Ranitidine, - Laser light can be focused on a
Famotidine bleeding point to induce rapid tissue
– Proton pump inhibitors healing
• Omeprazole, Lansoprazole, e. Electrocoagulation
Esomeprazole, Pantoprazole, - Endoscopic procedure
Rabeprazol - - Heat generated from high-
d. Cytoprotective frequency electrical current is
– Coats ulcer capable of coagulating or cutting
– prostaglandin synthesis - tissue
– Taken on an empty stomach (30 - 60 - Thermal electrocoagulation- classic
mins. before meals) treatment for bleeding during
– Eg., Carafate (Sucralfate) surgery and has recently been used
e. Side effects to treat GI bleeding.
– Antacids f. Angiographic therapy
• Magnesium based - diarrhea -- Radiological therapy when
• Aluminum based- endoscopy has failed to be
constipation cytotic antivicer drug
· :
diagnostic
– H2 Blockers - Considered for patient at high risk
• Diarrhea for surgical intervention
• Abdominal cramps - Embolic material such as an
• Confusion absorbable gelatin sponge, tissue
• Dizziness adhesives, or other occlusion
devices ( such as microcoils) can be
• Weakness
inserted through a catheter into the
area of bleeding.
Surgical remove
a. Vagotomy- resection of the -vagus nerve g. Injection Therapy
- Alternative to - heat therapy, is
– Decrease cholinergic stimulation à ¯
inexpensive, simple and widely
HCl secretion à ¯ gastric motility used
-
b. Pyroplasty- Surgical dilation of the pyloric - A catheter with a small retractable
sphincter
↑

dilation para
>
- madali

matransfer a duodenum needle is passed through the

• Improves gastric emptying of endoscope, and vessels are
acidic chyme - treated with one or more of several
c. Antrectomy- Removal of 50% of the lower different chemical agents.
part of the stomach
Management and hemorrhage. Gastric glands are intact
Nursing care at this stage. > -
(pasalim ng palalim)
mas malala

1. Assessment • Atrophic gastritis- inflammation

a. Hx (predisposing factors) extends deeper into the mucosa with
b. Objective data progressive glandular destruction.
1. s/s o Invariably present in pernicious
2. complications anemia.
2. Lifestyle modification o Characterized by decreased
a. DIET number of parietal and chief cells.
b. Smoking, ETOH • Hypergastritis or gastric atrophy-
c. Stress hemorrhage occur frequently.
3. Complications of Sx o Gastric glands undergo
a. Dumping syndrome transformation at this stage and
1. Nausea metaplastic changes are an
2. Sweating importantpredisposing factor for
3. Pallor gastric cancer.
b. Vertigo
1. Marginal ulcers Etiology
2. Paralytic Ileus paralyzed intestine
>
-

1. Ingestion of irritants
3. Hemorrhage a. Erosive
4. Acute gastric dilation
-

b. Corrosive
4. Pre-op
-

2. Microorganisms
a. NPO/ enema a. H. pylori infection
b. Consent b. Staph infection
c. Health teaching 3. Autoimmune
5. Post-op
a. Ambulation Predisposing Factors
b. NGT TPN IV
>
-
thr
·

1. Environmental factors
c. Nutrition a. Radiation, smoking
d. Complications 2. Pathophysiologic conditions
6. Nursing Diagnoses a. Burns, renal failure, sepsis
a. Acute/ chronic pain 3. Other factors
b. Imbalanced nutrition a. Psychologic stress (surgery, burns,
severe infection) • NG tube
Gastritis Assessment
Definition 1. Acute gastritis
• Inflammation of gastric mucosa a. Anorexia
• usually due to infectious agents (such as b. Nausea/ vomiting
Y
Helicobacter pylori) and
-
c. Epigastric Discomfort 4. Feeling of
• autoimmune and hypersensitivity reactions fullness
O
• Most common in clients 50-60 y/o
• Male
d. GI Bleeding
e. Common with alcohol abuse
f. May be only symptom
Types of Gastritis 2. Chronic gastritis
1. Acute -– short term inflammation a. Anorexia
2. Chronic -e long standing b. Nausea/ vomiting
• Superficial gastritis- inflammatory c. Epigastric Discomfort
changes are limited to the surface d. Feeling of fullness
mucosa, which causes an erythemic, e. Intolerance of spicy/ fatty food
edamatous mucosa with small erosions
Diagnosis • complications
1. Acute gastritis: diagnosis most often based b. Lifestyle modification
on history of -
drug and alcohol abuse 1. DIET (bland, decaf, small
2. Chronic gastritis: diagnosis may be delayed meals)
or missed due to nonspecific symptoms
-
2. Smoking, ETOH
a. Endoscopy 3. Stress
b. H. pylori tests c. Symptom Management
c. CBC 1. Pain
d. Guaiac 2. N/V
e. Gastric analysis d. Promote self-care
• Determines achlorhydria e. Health teaching
(lack of acid secretion) 1. Medication/ restrictions/ side
• Associated with severe effects
atrophic gastritis 2. Complications (S/Sx)
f. Serum antibody tests
g. Schilling test
h. Tissue biopsy Food Poisoning
i. Radiologic studies not helpful • Sudden illness that occurs after ingestion of
contaminated food or drink.
Complications • Botulism is a serious form of food poisoning
1. Bleeding that requires continual surveillance.
2. Pernicious anemia
3. Cancer Cause
• Contaminated food or drink
Management
1. Medical Management Signs and symptoms:
a. NPO (N/V) • Nausea and vomiting
b. NGT • Diarrhea Diagnostics:
c. Monitor bleeding • Food, gastric content, feces
d. Lavage of irritants • Serum electrolytes Medical Management:
e. Keep stomach empty
• Determining the source and type of food
f. Lifestyle changes poisoning
g. Diet
• Assess for signs of fluid and electrolytes
h. Alcohol
imbalance
i. Smoking
2. Pharmacologic Management • Assess for signs of hypovolemic shock
a. Antacids • Control nausea to prevent vomiting
• Pharmacological:

I
b. H2 blockers
c. PPIs • Anti-emetic medication Nursing
d. Antibiotics
e. Cobalamin pernicious animia Management:
f. Antiemetics • Monitor rr, bp, sensorium, vp (if indicated),
3. Surgical Management and muscular activity
a. Vagotomy • Encouraged the patient to take sips of weak
b. Pyloroplasty tea, carbonated drinks or tap water for mild
c. Gastrectomy nausea
4. Nursing Management • If vomiting subsides, clear liquids are usually
a. Assessment prescribed for 12 to 24 hrs then gradually
1. Hx (predisposing factors) progressed to low- residue bland diet.
2. Objective data
• s/sx
 FAR EASTERN UNIVERSITY
Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Endocrine-Metabolism

Disorders in GIT-Metabolism: Disturbances in Absorption and Elimination

Disorders of Intestinal Motility • Distention

1. Diarrhea • Intestinal rumbling
2. Constipation • Anorexia
3. Irritable Bowel Syndrome • Thirst
4. Fecal incontinence • Painful spasmodic contractions of the anus
• Tenesmus
Diarrhea
• Increased in frequency of bowel movements, Diagnostics:
increased amount of stool and altered • CBC

1
consistency of stool. • Urinalysis
• Is associated with urgency, perianal • Stool exams
discomfort, incontinence or a combination of
• Electrolytes
these factors.
• Endoscopy
• It occurs when fecal matter passes through
the intestine rapidly, resulting in decreased • Barium enema
• absorption of water, electrolytes, and
Complications:
nutrients and causing frequent, watery stools.
• Cardiac dysrhythmias ( atrial and ventricular
• Can be acute or chronic.
tachycardia, ventricular fibrillation, PVC)
Medical Management
Types:
a. Secretory
Medical Management
b. Osmotic
c. Mixed • Controlling the symptoms
• Preventing complications
Etiology: Bacterial and viral infection • Eliminating or treating the underlying disease

Causes: Pharmacological management

• Medications (e.g thyroid hormone • Antibiotics
replacement, stool softeners and laxatives, • Anti-inflammatory
antibiotics, chemotherapy, antacids) • Anti-diarrheal medications (diphenoxylate or
• Metabolic and endocrine disorders (e.g DM, loperamide)
Addison’s disease, thyrotoxicosis)
• Viral or bacterial infections (e.g dysentery, Nursing Management:
shigellosis, food poisoning) • Assessing and monitoring the characteristics
• Nutritional and malabsorptive disorders ( and pattern of diarrhea
celiac, anal sphincter defect, Zollinger • Encourage bed rest
Ellison syndrome, intestinal obstruction) • Increase oral fluid intake
• Bland low in bulk diet
Signs and Symptoms • Perianal care
• Increased frequency and fluid content of the
stools
• Abdominal cramps
 ·

Constipation • Fecal impaction

• Abnormal infrequency or irregularity of • Hemorrhoids and fissures
defecation, abnormal hardening of stools that • Megacolon
makes their passage difficult and sometimes
painful Medical Management:
• Decrease in stool volume or retention of stool • Education -
high
Givegive in Fiber , water

in the rectum for a prolonged period • Bowel habit training

• Interference with one of three major • Increase fiber and fluid intake
functions of the colon
I

• Judicious use of laxatives/ discontinuing

o Mucosal transport laxative use
o Myoelectric activity • Routine exercise
o Processes of defecation • Diet ( unprocessed bran)
Causes: Pharmacological management:
a. Medications ( tranquilizers, anticholinergics, • Cholinergic agent (e.g bethanecol)
anti-depressants, opioids, antacids with
• Cholinesterase inhibitors ( e.g neostigmine)
aluminum and iron)
b. Rectal or anal disorder ( hemorrhoids, • Prokinetic agent ( e.g metoclopramide)
fissures) • Enemas and rectal suppositories are generally
c. Obstruction ( cancer of the bowel) not recommended
d. Metabolic, neurologic and neuromuscular
conditions ( DM, Hirschsprung’s disease, Nursing Management:
Parkinson’s disease, multiple sclerosis) • Patient education
e. Endocrine disorders (hypothyroidism, • Health promotion Goal of treatment:
pheochromocytoma) • Restoring or maintaining a regular pattern of
f. Lead poisoning elimination
g. Connective tissue disorder (scleroderma, • Ensuring adequate intake of fluids and high
lupus erythematosus) fiber foods
• Relieving anxiety about bowel elimination
Signs and Symptoms: patterns
• Abdominal distention • Avoiding complications
• Borborygmus
• Pain and pressure Irritable Bowel Syndrome
• Decreased appetite • aka spastic colon, intestinal neurosis, spastic
• Headache colitis, irritable colon
• Fatigue • a functional bowel disorder of motility in the
• Indigestion intestine
• Sensation of complete emptying • chronic abdominal complaints without a
• Straining at stool structural or biochemical cause
• Elimination of small-volume, hard, dry stools • characterized by alternating periods of
constipation and diarrhea
Diagnostics:
• Barium enema Types:
• Diarrhea-predominant (IBS-D)
• Sigmoidoscopy
• Constipation-predominant (IBS-C)
• FOBT
• Anorectal manometry • Alternating diarrhea and constipation
o 20% Western Society, Mostly
• Defecography and bowel transit studies
Women
o No known cause
Complications:
• Hypertension
Etiology: 6. Referral
• abnormal communication between the enteric
nervous system and the central nervous Fecal Incontinence
system • involuntary passage of stool from the rectum
• exaggerated reaction to stimuli • can result from trauma, neurologic disorder,
• an imbalance of serotonin in the gut inflammation, infection, radiation, treatment,
• Serotonin fecal impaction, pelvic floor relaxation,
• intestinal motility perception of pain release laxative abuse, medications or advancing
of water age.

Irritable Bowel Syndrome Factors influence fecal incontinence

• Weight usually remains stable 1. Ability of the rectum to sense and
• Stools usually of small volume accommodate stool
• May have mucus but usually not blood 2. Amount and consistency of stool
3. Integrity of the anal sphincter and
Diagnosis 4. musculature
5. Rectal motility
• Stool culture, occult blood
• Endoscopy*
Signs and Symptoms:
• Barium Enema*
• Occasional urgency and loss of control
• CT Scan*
• Complete incontinence
* For differential diagnosis
• Poor control of flatus
Goals of treatment
Diagnostics:
• Relief of gastrointestinal symptoms
• Rectal examination
• Relief of psychological distress
• Flexible sigmoidoscoy
• Improve quality of life
• Barium enema
Management • CT scans
1. Lifestyle changes • Anorectal manometry
a. Decrease emotional stress • Transit studies
b. Diet modification limit coffee, tea,
chocolates increase fiber, frequent Medical Management:
small meals • Help the patient achieve a better quality of
2. Pharmacological Management life
a. Antispasmodics and anticholinergic • Bowel training program
b. Tricyclic antidepressants (Elavil)
c. Anxiolytics (Diazepam, Xanax) Surgical Management:
d. Laxatives with caution • Surgical reconstruction
• Sphincter repair
Nursing Management • Fecal diversion
1. Assessment
a. s/s Nursing Management:
b. Predisposing factors • Assist the patient in to achieve fecal
c. Prepare for procedures incontinence or
d. Hydration status • Manage the problem so the patient can have
e. Skin assessment predictable, planned elimination pattern.
f. Fecal impaction • Maintaining perineal skin integrity
2. Administer medication as necessary
3. Encourage fluids
4. Peri-anal care
5. Health Teaching
 Malabsorption Syndrome intestines removed, or rarely due to the
1. Sprue complete dysfunction of a large segment of
2. Short Bowel Syndrome bowel.
• People with short bowel syndrome cannot
Sprue absorb enough water, vitamins, and other
• e
Malabsorption occurs when the GI system is nutrients from food to sustain life.
unable to absorb one or more of the major
nutrients. Etiology
• Necrotizing enterocolitis in infant
Causes: • Congenital defects of the bowel, such as
• Ileal dysfunction • Midgut volvulus
• Jejunal diverticula • Omphalocele
• Parasitic disease • Gastroschisis
• Celiac disease • Jejunoileal atresia
• Enzyme deficiency • Internal hernia
• IBD • Short bowel
• Meconium ileus
The primary malabsorption disorders are: • Intussusceptions
• Tropical sprue • Crohn’s disease
• Adult celiac disease (non tropical sprue) • Bowel injury
• Lactose intolerance • Cancer
Medical and Nursing Interventions: Clinical Manifestations
1. Tropical sprue: Folic acid, broad spectrum • Diarrhea
antibiotics and a high calorie, high protein, • Fatigue
low fat diet
• Pale, greasy stools
2. Celiac disease: High calorie, high protein,
• Swelling ( edema) esp. legs
gluten free diet
3. Lactase Deficiency: Deficiency in lactase, an • Very foul smelling stools
enzyme that breaks down lactose (milk • Weight loss
sugar), causes lactose intolerance. When
lactose is not digested, a high concentration Diagnostic Tests
of it occurs in the intestines, causing an • Albumin level
osmotic retention of water in the colon and • CBC
watery stools. • Fecal fat test
• Small intestine x-ray
Medical and Nursing Interventions: • Vitamins levels in the blood
• Removing foods from the diet that contain
lactose such as milk and milk products Medical and Nursing Intervention
• Some fermented milk products such as milk 1. Nutritional support
and yogurt, may be lower in lactose and better a. Oral rehydration solutions, parenteral
• tolerated. nutrition, enteral nutrition, and
• Lactaid – digests 70% of the lactose in foods medications
making them more tolerable. b. SFF, fluid and and nutritional
supplementation and medications to
Short Bowel Syndrome address diarrhea for mild case
• Also known as short gut syndrome or simply c. Additional IV fluids and electrolytes
short gut supplements as needed for moderate
case
• A group of problems related to poor
d. Parenteral nutrition and oral
absorption of nutrients that typically occurs
in people who have had half or more of their rehydration solutions for severe case
 • IRREDUCIBLE or INCARCERATED-
Structural and Obstructive Bowel Disorder adhesions or edema occur between the sac
1. Hernia and its contents. The trapped loop of bowel
2. Intestinal Obstruction becomes strangulated with the blood supply
a. Small Bowel Obstruction cut off.
b. Large Bowel Obstruction
3. Diverticulosis (Hernia) Therapeutic Interventions:
• Hernias are diagnosed by physical
Hernia examination
• Abnormal protrusion of an organ or structure • A supportive truss or brief applies pressure to
through a weakness or tear in the wall of the keep the reduced hernia in placed.
cavity normally containing it, which in this • Surgery is recommended for inguinal hernias
case is the abdominal wall. and is indicated if there is strangulation or the
• The hernial sac is formed by the peritoneum threat of bowel obstruction.
protruding through the weakened muscle • For symptomatic hernias, surgical procedures
wall. includes open hernia repair ( herniorrhapy) or
• Contents of the hernia can be small or large hernioplasty ( open or laparoscopically)
intestine or the omentum. • Bowel resection or a temporary colostomy
maybe necessary if the hernia is strangulated.
Indirect hernias- caused by a defect of structural
closure. Herniorrhaphy- involves making an incision in the
abdominal wall, replacing the contents of the hernia
Direct hernias- acquired and arise from a weakness sac, sewing the weakened tissue, and closing the
in the abdominal wall, usually at old opening.
site.
Hernioplasty- involves replacing the hernia into the
Types of Hernias: abdomen and reinforcing the weakened muscle wall
• Inguinal hernias- located in the groin where with wire, fascia or mesh.
the spermatic cord in males or the round
ligament in females emerges from the Intestinal Obstruction
abdominal wall. This common hernia is an
example of an indirect hernia and is usually Small bowel obstruction
seen in males • When obstruction occurs in the small bowel,
• Umbilical hernias- are seen most often in a collection of intestinal contents, gas, and
obese women and children. They are caused fluid occurs proximal to the obstruction.
by a failure of the umbilical orifice to close. • The distention that results stimulates gastric
• Ventral (incisional) hernias- result from a secretion but decreases the absorption of
weakness in the abdominal wall following fluids.
abdominal surgery, especially in the obese • As distention worsens, the intraluminal
patient, if a drainage system was used , the pressure causes a decrease in venous and
patient experienced poor wound healing or arterial
the patient received inadequate nutrition. • capillary pressure, resulting in edema,
necrosis, and eventually perforation of the
Clinical Manifestations: intestinal wall.
• Abnormal bulging can be seen in the affected
area of the abdomen, especially when Etiology: overdistention
straining or coughing. It may disappear when • Abdominal surgery and trauma
the patient lies down. • Pneumonia
• REDUCIBLE HERNIA- intestinal mass • Spinal injuries
easily returns to the abdominal wall or • Hypokalemia
manually placed back in the abdominal cavity
• Myocardial infarction
 • Peritonitis Etiology
• Vascular insufficiency • Carcinoma
• IBD
Clinical Manifestations: • Diverticulitis
• Wavelike abdominal pain and vomiting • Benign tumors
• Flatus and feces that are low in the bowel and • Impaction
blood and mucus may be passed
• Fecal vomiting Clinical Manifestations:
• Peristaltic waves may be visible in thin • Constipation if the obstruction is in the
person rectum or sigmoid colon.
• Pain that is sharp and sustained may indicate • As the loop of bowel distends, the patient
perforation may complain of crampy lower abdominal
• In mechanical obstructions, high pitched, pain and
tinkling bowel sounds are heard proximal to • abdominal distention.
the • Vomiting, if it occurs, is a late sign and
• obstruction and are absent distal to it. maybe fecal
• If the obstruction is non mechanical, there is • High pitched tinkling bowel sounds maybe
an absence of bowel sounds. heard
• Dehydration due to loss of F&E • A localized tender and mass maybe felt on
• The lower in the gastrointestinal tract the palpation
obstruction is, the greater the abdominal • Large bowel obstructions, if not diagnosed
distention. and treated, can lead to gangrene, perforation,
• An uncorrected obstruction can lead to shock and peritonitis.
and possibly death.
Diagnostic Test:
Diagnostic Tests : • Radiological examination reveals a distended
• Radiographic studies and CT scans- will colon.
reveal dilated loop loops of bowel
• Leukocytosis is evident if strangulation and Medical and Nursing Interventions:
perforation occurs. • Enemas and manual disimpaction maybe
• Hgb and Hct levels elevated effective if impaction is present
• Serum electrolytes decreased • Surgical intervention for mechanical
blockages
Medical and Nursing Interventions: • Surgical resection of the obstructed colon
·

• NPO and bowel decompression using NGT maybe necessary

• IVF therapy • A temporary colostomy may be indicated to
• Sometimes IV antibiotics allow the bowel to rest and heal.
• Surgical intervention for complete • Ileonal anastomosis is sometimes done
mechanical obstruction • Cecostomy for patient with poor surgical risk
to allow diversion of stool.
Large Bowel Obstruction Less common
=

• Obstruction in the large bowel is less Diverticulosis (Hernia)

common and not usually dramatic as small • small pouches in the colons that bulge
bowel obstruction. outward through weak spots, like an inner
• Dehydration occurs more slowly because of tube that pokes through weak places in a tire
the colon’s ability to absorb fluid and distend pouch is called the diverticulum
well beyond its normal full capacity. • condition becomes more common as people
• If the blood supply to the colon is cut off, the age
patient’s life is in jeopardy because of bowel
-
• Diverticulosis and diverticulitis are also
strangulation and necrosis. called diverticular disease
 • Most people with diverticulosis never have • Avoidance of nuts, popcorn, and sunflower,
any discomfort or symptoms. • pumpkin, caraway, and sesame seeds
• The most likely cause of diverticulosis is a • Pain medication – if with cramps, bloating or
low-fiber diet because it increases constipation
constipation and pressure inside the colon.
Diverticulitis
Signs and Symptoms • on clearing up the infection and
• Most people with diverticulosis do not have inflammation,
any discomfort or symptoms mild cramps • resting the colon, and preventing or
• bloating minimizing
• Constipation • complications
• For diverticulitis: • Antibiotics
• Abdominal pain • rest and a liquid diet, along with a pain
reliever
Causes • Hospitalization if with severe attack or pain
• Bleeding – rare complication, can sometimes • Possible surgery
be severe but may stop by itself and not
require treatment When is surgery needed?
• Abscess, perforation, and peritonitis - an • If attack is severe or frequent
infected area with pus that may cause • surgeon removes the affected part of the
swelling and destroy tissue colon
o infected diverticula may develop • and joins the remaining sections (colon
small holes, called perforations • resection)
• Fistula - abnormal connection of tissue • large abscess, perforation, peritonitis, or
between two organs or between an organ and • continued bleeding
the skin
o when tissues comes into contact with Anorectal Disorders
each other during infection, they stick 1. Hemorrhoids
together, if heal this way, fistula will 2. Anal fissures
result 3. Appendicitis
o most common occurs between the
bladder and colon Hemorrhoids
• Intestinal Obstruction – scarring may cause • veins around the anus or lower rectum are
partial or total blockage of the large intestine swollen and inflamed
o the colon is unable to move bowel
• may result from straining to move stool
contents normally
• either inside the anus—internal—or under
the skin around the anus—external
Causes
• common in both men and women
• Low fiber diet
• half of the population has hemorrhoids by age
• Constipation
50
Diagnosis • contributing factors include pregnancy,
aging, chronic constipation or diarrhea, and
• Medical History– bowel habits, symptoms,
anal intercourse
pain, diet and medication
• Physical Assessment– digital rectal exam Signs and Symptoms
• Diagnostics– e.g. stool exam and X-ray • red blood covering the stool,↑
on toilet paper,
or in the toilet bowl
Treatment for Diverticulosis
• Painful and irritation of the protruded part
• High fiber diet – with exercise
• Taking of Citrucel or Metamucil once a day
 • painful swelling or a hard lump around the Appendicitis
anus that results when a blood clot forms • Inflammation of the appendix, the small,
(thrombosed external hemorrhoid) fingerlike appendage attached to the cecum
of the large intestine.
Diagnosis Because of the small size of the appendix,
• Physical examination obstruction may occur, making it susceptible to
• Uses anoscope and proctoscope for better infection.
visualization The resulting inflammatory process causes an
increase in intraluminal pressure of the appendix.
Treatment/Interventions
• Tub baths/Hot Sitz Clinical Manifestations:
• Application of hemorrhoidal cream or • Fever, increased WBC, and generalized pain
suppository in the upper abdomen
• Increasing fiber and fluids • Within hours of onset the pain usually
• Stool Softeners becomes localized to the right lower quadrant
• Rubber band ligation- A rubber band is at McBurney’s point, midway between the
placed around the base of the hemorrhoid umbilicus and the right iliac crest.
inside the rectum. The band cuts off • Nausea, vomiting, and anorexia are also
circulation, and the hemorrhoid withers away usually present.
within a few days. • PE reveals slight abdominal muscular rigidity
• Sclerotherapy- A chemical solution is (guarding), normal bowel sounds, and local
injected around the blood vessel to shrink the rebound tenderness (intensification of pain
hemorrhoid. when pressure is released after palpation) in
• Infrared coagulation- A special device is themright lower quadrant of the abdomen.
used to burn hemorrhoidal tissue. • Pain in the right lower quadrant when the left
• Hemorrhoidectomy - Occasionally, lower quadrant is palpated (Rovsing’s sign)
extensive or severe internal or external
hemorrhoids may require removal by surgery Diagnostic Tests:
• A complete blood cell count (CBC) reveals
Anal Fissures elevated leukocyte and neutrophil counts.
• Cracks or ulcers in the lining of the anal canal • UTZ or Ct scan reveals an enlargement in the
• Most commonly associated with constipation area of the cecum.
and stretching of the anus with passage of
hard Medical and Nursing Management:
• stool, although Crohn’s disease or other • The patient is kept NPO and surgery is done
factors may also play a role. immediately unless there is evidence of
• The patient may experience bright red perforation or peritonitis.
bleeding. • Ice to the site of pain and maintaining semi-
• Pain may also be so severe that the patient fowler’s position may help reduce pain while
delays defecation, leading to further the diagnosis is being made.
constipation • If the appendix has ruptured, IV fluids and
• and worsening of symptoms. antibiotic therapy are started and surgery may
be delayed for 8 hrs or more.
• Treatment of anal fissures involves measures
to ensure soft stools, allowing fissures time to • After surgery, the patient is usually NPO until
• heal. GI functioning returns, and if the appendix
has ruptured, the patient may have and NGT
• Sitz bath may be used to promote circulation
placed to decompress the stomach.
to the area to aid in healing.
• When bowel function returns, initial diet
consists of clear fluids and is advanced as
tolerated by the patient.
• Vital signs and abdominal data are collected
to monitor for signs and symptoms of
peritonitis.
• Pain control to promote early ambulation,
coughing, deep breathing, and turning help
prevent respiratory complications.
 FAR EASTERN UNIVERSITY
Institute of Nursing
A.Y 2020 – 2021 Second Semester
Medical-Surgical Nursing 2
Endocrine-Metabolism
Module 2 Care of Clients with Endocrine Disorders
Review of Anatomy, Physiology, and Functions of the Endocrine System

Outline: functions, the hormonal system & regulates

1. Review of Anatomy, Physiology, and sleep and stimulates appetite
Functions • Secretes hypothalamic hormones
a. Endocrine Glands
b. Functions PITUITARY GLAND
c. Sources of Hormones and related • Approximately the size of a pea.
disturbances • It hangs by a stalk from the inferior surface of
the hypothalamus.
THE ENDOCRINE SYSTEM • It has two functional lobes:
The second great controlling system of the body. o Anterior pituitary
• It coordinates and directs the activity of the o Posterior pituitary
body’s cells
• It allows communication within the distant Anterior Pituitary Gland
sites of the body • Follicle Stimulating hormone
• A collection of glands that produce hormones • Luteinizing Hormone
that regulate the body’s growth, metabolism • Adrenocorticotropic Hormone
and sexual development and function. • Thyroid Stimulating Hormone
• Hormones are released into the bloodstream • Growth Hormone
and transported to tissues and organs • Prolactin
throughout the body.
Posterior Pituitary Gland
Three Components of the Endocrine System • Oxytocin
1. Endocrine glands
• Antidiuretic Hormone
2. The Chemical Messengers called
HORMONES
THYROID GLAND
3. Target cells or organs
• Produces hormones that stimulate body heat
production, bone growth, and the body’s
ENDOCRINE GLANDS
PINEAL BODY metabolism.
to ty thyrocalcitonin
• A small cone- shaped gland that hangs from
, ,

ADRENAL GLANDS
the roof of the third ventricle of the brain.
• Secretes hormones that influence the body’s
• Secretes melatonin which is believed to be a
metabolism, blood chemicals & body
“sleep trigger”
characteristics
HYPOTHALAMUS • Influence the NS involved in the response &
defense against stress.
• Is a small area of the brain located in the
section of the forebrain called the
PANCREAS
diencephalon.
• Secretes a hormone (insulin) that controls
• It is concerned with homeostasis.
the use of glucose by the body.
• Activates and controls the part of the nervous
system that controls involuntary body OVARIES AND TESTICLES
 • Secretes hormones that influence female and • Oxytocin- Contracts pregnant uterus, milk
male characteristics ejection from breast after childbirth

FUNCTIONS OF THE ENDOCRINE SYSTEM ADRENAL CORTEX

1. Maintainance and regulation of vital • Mineralocorticoids (aldosterone)- ­ Na
functions reabsorption, K- loss by the kidney
2. Response to stress and injury • Glucocorticoid (cortisol)- influences
3. Growth and development metabolism of all nutrients; regulates blood
4. Energy metabolism glucose, affects growth, has anti-
5. Reproduction inflammatory action, and decreases effects of
6. Fluid, electrolyte and acid-base balance stress
• Androgen- Androgenistic activity
SOURCES OF HORMONES
HYPOTHALAMUS ADRENAL MEDULLA
Hormones: • Epinephrine and Norepinephrine-
• Releasing or Inhibiting Hormones neurotransmitters of the CNS
• Corticotropin-releasing hormone (CRH)
• Thyrotropin-releasing hormone (TRH) THYROID GLAND (FOLLICULAR CELLS)
• Growth hormone-releasing hormone • Thyroid Hormones: triiodothyronine (T3),
(GHRH) Thyroxine (T4)
• Gonadotropin-releasing hormone (GnRH) o ­ metabolic rate; ­CHON and bone
turnover; ­ responsiveness to
Functions: catecholamines; important for fetal
• Controls the release of pituitary hormones and infant growth and development

ANTERIOR PITUITARY GLAND PARATHYROID GLANDS

• Growth Hormone (GH)- Stimulates growth • Calcitonin- ¯ Blood calcium
of bone and muscle, promotes protein • Parathyroid hormone- regulates calcium in
synthesis and fat metabolism, ¯ CHO the blood
metabolism
• Adrenocorticotropic Hormone (ACTH)- PANCREATIC ISLET CELLS
Stimulates synthesis and secretion of adrenal • Insulin- ¯ Blood glucose by facilitating
cortical hormones glucose transport across cell membranes of
• Thyroid-stimulating hormone (TSH)- the muscle, liver, and adipose tissue
Stimulates the synthesis and secretion of • Glucagon- ­ blood glucose concentration by
thyroid hormone stimulation of glyconolysis and
• Follicle-stimulating hormone (FSH) glyconeogenesis
o Females: growth of ovarian follicle • Somatostotin- delays intestinal absorption of
for ovulation glucose
o Males: sperm production
• Luteinizing Hormone (LH) OVARIES
o Females: development of corpus • Estrogen- development of sex organs and
luteum, release of oocyte, production sex characteristics
of estrogen and progesterone • Progesterone- influences menstrual cycle;
o Males: secretion of testosterone, stimulates growth of uterine wall; maintains
development of interstitial tissue of pregnancy
testes • Inhibin- inhibits FSH secretion by the
anterior pituitary
POSTERIOR PITUITARY GLAND
• Antidiuretic Hormone (ADH)- ­ Water TESTES
reabsorption by the kidney
 • Androgens: testosterone- Develops males sex § X ovulation
organ and secondary sex characteristics; § X menstruation
sperm production § Infertility
• Inhibin- inhibits FSH secretion by the MSH (Melanocyte – Stimulating Hormone)
anterior pituitary • Hypersecretion “Eternal tan” / bronze
appearance of the skin
PLACENTA • Hyposecretion Albinism
• Human Chorionic Gonadotropin-
maintains pregnancy ANTERIOR PITUITARY GLAND
(Neuropophysis)
ADIPOSE TISSUE ADH (Antidiuretic Hormone) Diagnosticaodium <135 mea/Lo
-
osmolarity
• Hypersecretion- SIADH
Low
rosnol/leg
• Leptin- decreases appetite and food intake, ­
serom
> noo
Irvine osmolarity
vrive sodium
↓ high

(mor
o Edema, wt. Gain disorder
·

sympathetic activity and metabolic rate, cause due to >

-
fluid ·
maintain balares

o HPN
-

Restriction of
¯insulin secretion to ¯ fat storage
·

water

excessive ·
maintain sodium balance

• Resistin- suppresses insulin’s ability to o Dilutional hyponatremia

stimulate glucose uptake by adipose cells • Hyposecretion: Diabetes Insipidus WOF dehydration shock >
- :
,

Risk for fall

>
o Polyuria
-

DISTURBANCES RELATED TO HORMONES o Retarded growth

ANTERIOR PITUITARY GLAND o Dehydration
(Adenohypophysis) o Constipation
Growth hormone (Somatotropin) o Dilute urine, ¯ sp. gr.
• Hypersecretion:
o Children- Gigantism Oxytocin
o Adult – Acromegaly
• Hyposecretion: Dwarfism THYROID GLAND
• T3 (Triidothyronine)- Metabolism, growth
Prolactin (Mammotropic / Lactotropic Hormone) • T4 (Thyroxine)- Catabolism, body heat
• Hypersecretion – Galactorrhea production
• Hyposecretion - X milk during lactation • Thyrocalcitonin- Regulates serum Ca levels

ACTH (Adrenocorticotropic Hormone) DIAGNOSTIC TESTS

• Hypersecretion - Sec. Cushing’s Disorder 1. T3 T4 levels regulate thywid stimulating hormone
-

Hyposecretion - Sec. Addison’s Disorder • ­- hyperthyroidism T3 : normal value -

• ¯ - hypothyroidism T4 :
-

PITUITARY GLAND (Hypophysis) 2. PBI (Protein – Bound Iodine)

TSH (Thyroid – Stimulating Hormone) • Preparation: X Foods, drugs, test dyes
• Hyposecretion – Sec. Hyperthyroidism with iodine& 7 – 10 days before the test
• Hypersecretion - Sec. Hypothyroidism 3. RAIU (Radioactive I Uptake)
• Tracer dose of I131, p.o.
Gonadotropin (FSH / LH) • 2°, 6°, 24° ® exposure to scintillation
• Hypersecretion – Precocious Puberty camera
• Hyposecretion • Preparation: X Foods, drugs, test dyes
o Males: with I 7 – 10 to days before the test
§ Small phallus and testicles • Temporarily discontinue
§ X growth of body hair contraceptive pills
§ ¯ Libido • ­ Uptake – hyperthyroidism
§ Impotence • ¯ Uptake – hypothyroidism
§ Aspermia 4. Thyroid Scan
o Females: • Radioisotope / IV
§ Failure to develop the breasts • Exposure to scintillation camera
§ X growth of body hair
5. FNB (Fine Needle Biopsy)
6. BMR (Basal Metabolic Rate) – Measures
O2 consumption at the lowest cellular
activity
• Preparation
o NPO 10 – 12°
o Night Sleep 8 - 10°
o X get up from the bed the
following morning until the
test is done • A device with a
nose clip and a mouthpiece is
used; the client performs deep
breathing exercises
• Normal : ± 20% (euthyroid)
7 Reflex testing (kinemometry)
.
 Disorder of
pituitary
① Diabete
Insipdus

FAR EASTERN UNIVERSITY

Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Endocrine-Metabolism
Disorders Related to the Endocrine System

Outline: 4. Antithyroid drugs

• Disorders of the thyroid glands
o Hypothyroidism Pathophysiologic Mechanisms
o Hyperthyroidism • Decreased metabolic rate (due to
• Disorders of the parathyroid gland hyposecretion of T3)
o Hypoparathyroidism • Decreased body heat production (due to
o Hyperparathyroidism hyposecretion of T4)
• Disorder of the Pancreas • Hypercalcemia (due to hyposecretion of
o Diabetes Mellitus thyrocalcitonin
o Hypoglycemia
o Diabetic Ketoacidosis Clinical Manifestations:
• Disorders of the Adrenal Glands • Hair loss
o Addison’s Disease • Apathy
o Cushing’s Syndrome • Lethargy
o Conn’s Disease • Dry skin (coarse and scaly)
• Muscle aches & weakness
DISORDERS OF THE THYROID GLANDS • Constipation
Thyroid glands- produces Triiodothyronine (T3), • Intolerance to cold
Thyroxine (T4) that stimulate body heat production,
• Receding hairline
one growth, and the body’s metabolism.
• Facial and eyelid edema
Thyrocalcitonin (Calcitonin)- lowers serum Ca • Dull-blank expression
• Extreme fatigue
Goiter is an enlargement of the thyroid gland. • Thick tongue- slow speech
This is due to increased amount of TSH. It can be • Brittle hair and nails
associated with hyperthyroidism, • Menstrual disturbances
hypothyroidism and eurothyroidism.
Late clinical Manifestations:
Thyroid Gland Disorders: • Subnormal temperature
• Hypersecretion: hypothyroidism • Bradycardia
• Hyposecretion: hyperthyroidism • Decreased level of consciousness
• Thickened skin
HYPOTHYROIDISM • Cardiac complications

⑧
• Myxedema is hypothyroidism in adults.
• Cretinism is hypothyroidism in children. *Everything is low, slow, and dry.

Etiologies: Nursing Management:

1. Autoimmune (i.e. Hashimoto’s disease, 1. Monitor VS. Be alert for signs and symptoms
associated with recurrent respiratory of cardiovascular disorders
infections) 2. Diet: Low caloric, high fiber
2. Surgery (thyroidectomy) 3. Provide warm environment during cold
3. Radioactive Iodine therapy climate.
 4. Monitor weight. • Fine straight hair
5. Instruct client to avoid foods that inhibit • Bulging eyes
thyroid secretion: strawberries, peaches, • Facial flushing
pears, cabbage, turnips, spinach, cauliflower, • Enlarged thyroid
radishes, peas. • Tachycardia
• Increased systolic bp
Pharmacotherapy
• Breast enlargement
• Synthroid, Levothroid, Levoxyl
• Weigh loss
(Levothyroxine)
• Muscle wasting
• Cytomel (Liothryonine), Thyrolar (Liotrix),
• Finger clubbing
Thycar (Thyroid)
• Tremors
• BP, PR before administration.
• Diarrhea
• Start with low dose, gradually increase.
• Menstrual changes (amenorrhea)
• Should be given at least four hours apart from
multivitamins, antacids, bile acid • Localized edema
sequestrants, iron.
*These drugs decrease absorption of thyroid *Everything is high, fast, and wet.
replacement.
Ophthalmopathy
Myxedema Coma- an extreme, severe stage of • Exophthalmos is the protrusion of the
-

hypothyroidism. eyeballs. Caused by the accumulation of

• Can be precipitated by acute illness, rapid fluids at the fat pads behind the eyeballs,
withdrawal of thyroid hormones, anesthesia, pushing the eyeballs forward. This is
surgery, hypothermia, use of sedatives and irreversible. May lead to blindless.
narcotics. • Von Graefe’s sign (lid lag)- long and deep
-

palpebral fissure when one looks down

• S/Sx: hypotension, bradycardia,
hypothermia, hypoglycemia, hyponatremia, • Jeffrey’s sign- forehead remains smooth
-

respiratory failure, coma when one looks up

• Dalrymple’s sign (Thyroid Stare)- bright –
-

HYPERTHYROIDISM eyed stare, infrequent blinking

Common cause is Grave’s disease, also known as
toxic diffuse goiter. Associated with severe Nursing Management:
emotional stress, secondarily to autoimmune 1. Rest. Non – stimulating cool environment
-

disorders. 2. High caloric diet. Low fiber if with diarrhea.

-

3. Promote safety
4. Protect the eyes
-

Pathophysiologic Mechanisms
1. Artificial tears at regular intervals
-

• Increased metabolic rate (hypersecretion of

T3) 2. Wear dark sunglasses when going out
• Increased body heat production under the sun.
(hypersecretion of T4) 5. Replace fluid – electrolyte losses
• Hypocalcemia (hypersecretion of
Medical Management:
thyrocalcitonin)
Pharmacotherapy
1. Iodides: Lugol’s solution, Saturated
Thyroid hormones enhance actions of epinephrine
Solution of Potassium Iodide (SSKI)
and norepinephrine, increasing sympathetic activity.
Hypocalcemia results to increased cellular • To inhibit release of thyroid.
membrane permeability, leading to increased •- -
Mix with fruit juice with ice or glass
neuromuscular irritability. of water, with drinking straw
2. Thioamides: Tapazole (Methimazole), PTU
Clinical Manifestations: (Propylthiouracil)
• Intolerance to heat
 • To inhibit synthesis of thyroid Recurrent laryngeal nerve damage, Thyroid
hormones. storm, Myxedema
• Side effects: Agranulocytosis
(Neutropenia) Thyroid storm
3. Beta-blocker: Inderal (Propranolol) to • An uncontrolled and potentially life-
control tachycardia and hypertension threatening hyperthyroidism. It can occur
4. Ca – channel blockers, dexamethasone to from release of thyroid hormone into the
inhibit the action of thyroid hormones bloodstream during surgery, it can also
follow severe infection and stress.
Radiation Therapy • S/Sx hyperthermia, tachycardia,
• Radiation therapy (I131) dysrhythmias, systolic hypertension, nausea,
• Place client on isolation for few days. Body vomiting, diarrhea, restlessness, agitation,
secretions are radioactive-contaminated. irritability, delirium, coma
• Do not use in pregnant women because of
potential teratogenic effects. Pregnancy DISORDERS OF THE PARATHYROID
should be delayed for 6 months. GLANDS
Subtotal thyroidectomy Parathyroid Glands
• 5/6 of the gland is removed. • Produce parathormone (PTH)
• Low serum calcium levels stimulate PTH
Pre-operative Care release.
1. Promote euthyroid state (Control of thyroid • The relationship of PTH and calcium is direct
proportion, while PTH and phosphorus is
-

disturbance, Stable VS, Assess electrolyte -

levels, hyperglycemia, glucosuria). inverse.

2. Administer Iodides as ordered to reduce the
size & vascularity of thyroid gland, thereby Parathyroid Disorders
preventing postop hemorrhage and thyroid
crisis
3. Electrocardiogram (ECG) to evaluate cardiac
O 8
• Hyposecretion: Hypoparathyroidism
• Hypersecretion: Hyperparathyroidism

damage resulting from HPN and tachycardia. HYPOPARATHYROIDISM

• Abnormally low serum calcium levels
Post-operative Care (hypocalcemia), abnormally high phosphate
-
-

1. Position: Semi – Fowler’s with head, neck & levels (hyperphosphatemia), and
shoulder erect.
-

neuromuscular hyperexcitability (tetany).

2. Prevent Hemorrhage-- Ice collar over the neck • Acute Hypoparathyroidism is caused by
3. Keep tracheostomy set available for the first
-

accidental damage to parathyroid tissues

-48 hour postop. during thyroidectomy.
Parathyroid damage → HypoCa → • Chronic Hypoparathyroidism is usually
Laryngospasm → Airway obstruction -

idiopathic, resulting in lethargy; thin , patchy

4. Ask the patient to speak every hour to assess hair; brittle nails, scaly skin and personality
for recurrent laryngeal nerve damage changes.
5. Keep Calcium gluconate readily available.
Tetany occurs if hypoCa is present. Etiologies
6. -Monitor temperature. Hyperthermia is an 1. Iatrogenic- caused by accidental removal of
initial sign of thyroid crisis or trauma to parathyroid glands during
7. -Monitor BP. To assess for Trousseau’s sign thyroidectomy, parathyroidectomy or radical
(carpal spasm) (hypocalcemia). head or neck surgery.
8. -Steam inhalation to soothe irritated airways. 2. Autoimmune genetic dysfunction (affects
9. Advise to - support neck with interlaced more women than men).
fingers when getting up from bed 3. A reversible form may be associated with
10. Observe for signs of potential complications: hypomagnesemia, which interfere with PTH
Hemorrhage, Airway obstruction, Tetany, secretion.
Clinical Manifestations • Administer calcium supplement and Vitamin
Acute D. Vitamin D enhances calcium absorption
• Anxiety and irritability from GI tract.
• Numbness, tingling and cramps in the
extremities HYPERPARATHYROIDISM
• Dysphagia • Caused by overactivity of one or more of the
• Evidence of neuromuscular hyperexcitability: parathyroid glands. Usually occurs in clients
(+) Chvostek’s sign, (+) Trousseau’s signs, 60 years of age, and those with renal failure.
carpopedal spasms, bronchospasms, laryngeal Affects women twice as men.
spasms, arrythmias and convulsions • Primary hyperparathyroidism develops
• Hyperactive deep tendon reflexes (DTRs when the normal regulatory relationship
between serum calcium levels and PTH
Chronic: secretion is interrupted.
• Lethargy • Secondary hyperparathyroidism occurs
Thin patchy hair Brittle nails when the glands are hyperplastic because of
Dry and scaly skin Personality changes malfunction of another organ system usually
• Ectopic or unexpected calcification may the result of renal failure but may also occurs
appear in the eyes and basal ganglia as a result of cancer which includes multiple
myeloma, carcinoma with bone metastasis.
Nursing Management • Tertiary hyperparathyroidism occurs
1. Intervene for life-threatening tetany as when PTH production is irrepressible
indicated. (autonomous) in clients with normal or low
a. Administer IV Calcium gluconate to serum calcium levels.
prevent calcium depletion
b. Be alert for possible laryngeal spasm Clinical Manifestations
resulting respiratory obstruction, • fatigue, muscular weakness, restlessness
keep a tracheostomy set available. • height loss and frequent fractures
c. Institute seizure precautions as per • renal calculi
hospital protocol (padded side rails • anorexia, nausea, abdominal discomfort,
and bite blocks are controversial). constipation memory impairment,
d. Minimize environmental stimuli. depression,
2. Provide care for chronic hypoparathyroidism • psychoses
a. Encourage diet high in Calcium and • polyuria, polydipsia back and joint pain
low in phosphorus. Milk, milk
products and egg yolks must be *Bones, stones, moans, and groans
avoided because they are high in
phosphorus. Nursing Management:
b. Administer Vitamin D and 1. Prepare client for surgical treatment:
Magnesium Supplementation, as Parathyroidectomy.
indicated. In clients receiving 2. Prevent dehydration, constipation, kidney
magnesium, observe for symptoms of stone formation.
hypermagnesemia 3. Reduce added calcium by eliminating over-
c. Administer oral calcium preparations the-counter antacids.
to supplement the diet. 4. Assess for renal calculi: report hematuria or
flank pain as necessary.
Pharmacotherapy 5. Increase fluid intake and normal saline IV as
• Administer phosphate binder (Amphogel) to prescribed. 6. Administer Furosemide to
lower phosphorous level and increase serum lower serum calcium levels.
calcium. 6. Administer Calcitonin (Calcimar) to decrease
skeletal calcium release and increase renal
clearance of calcium.
 7. Administer antihypercalcemic: Gallium Insulin
nitrate (Ganite) • Produced by the beta cells of the islets of
Langerhans.
DISORDERS OF THE PANCREAS • Increases glycogenesis (breakdown of
Overview of Pancreatic Hormones glycogen into glucose for cellular energy use)
• The endocrine pancreas produces hormones • Increases fatty acids synthesis
necessary for the metabolism and cellular • Decreases glycogenolysis, gluconeogenesis
utilization of carbohydrates, proteins, and (generation of glucose from non-CHO
fats. substrates) and ketogenesis (breakdown of
• The cells that produce these hormones are fatty acids).
clustered in groups of cells called the Islets
of Langerhans. These islets have three Physiology
different types of cells. • some of the food breaks down into sugars-
one of these sugars is glucose, the body’s
Cells Produced by the Pancreas main fuel
• Alpha Cells- produce the hormone • Sugar enters the bloodstream, and the level of
glucagon, which stimulates the breakdown of sugar in your blood begins to rise
glycogen in the liver, the formation of CHO • When your body senses an increase in sugar,
in the liver, and the breakdown of lipids in it sends a signal to your pancreas
both the liver and adipose tissue. The primary • The pancreas make insulin and sends it into
function of glucagon is to decrease glucose the bloodstream
oxidation and to increase blood glucose • Insulin is the key that opens an “entrance”
levels. It prevents blood glucose from into the body’s cells and allows sugar to pass
decreasing below a certain level when the from the bloodstream into the cells
body is fasting or in between meals. • The level of sugar in the bloodstream falls as
• Beta Cells– secrete the hormone insulin, the sugar passes into the cells
which facilitates the movement of glucose
• The body’s cells use the sugar for fuel/
across the membranes into cells, decreasing energy
blood glucose levels. Insulin release is
regulated by blood glucose; it increases when Predisposing Factors
blood glucose levels increase, and it 1. Stress stimulates secretion of epinephrine,
decreases when blood glucose decreases. norepinephrine and glucocorticoids. These
• Delta Cells– produce somatostatin which is hormones elevate blood glucose levels.
believed to be neurotransmitter that inhibits 2. Heredity is associated with type II DM.
the production of both glucagon and insulin. 3. Obesity. Adiposes tissues are resistant to
• PP Cells- (F Cells) secretes pancreatic insulin, hence, cellular glucose uptake is
polypeptides- self regulate the pancreas poor.
secretion activities (endocrine and exocrine) 3. Viral infections increase the risk of
autoimmune disorders that may affect
DIABETES MELLITUS pancreas.
• From the Greek diabainein, “to pass 4. Autoimmune disorders which are
through,” describes the copious urination, associated with type I DM.
and mellitus, from the Latin, “sweetened with 5. Women who are multigravidas with large
honey,” refers to sugar in the urine. babies. During pregnancy, human placental
• It is a chronic disorder of carbohydrate, fat, lactogen (HPL) is produced. HPL
protein metabolism. antagonizes insulin, thus, hyperglycemia
• Characterized by elevated blood glucose occurs.
levels (hyperglycemia).
• Related to defects in insulin production/
secretion, impaired insulin utilization/ action
or both.
-

-
-

Oral
 observed for :
Gl -

upset
hypoglycemia
-

4
. near
sout shoes

HHS 5 X
yo bangoofed
.

lotion to feet
apply
thim fotrails right across

.
8 exercise
. X
9 near kew high Hocking
Types of Diabetes Mellitus
Type 1 DM Type 2 DM
• Insulin Dependent • Non-Insulin
Diabetes Mellitus Dependent Diabetes
• Juvenile-onset Mellitus
• Brittle or unstable • Maturity-onset
DM Onset if before • Ketosis-resistant DM
30 years old • Onset is after 30 years
• Absolutely deficient old
in insulin due to the • Relative lack of
absence of islets of insulin or resistance
Langerhans to the action of insulin
• Client is thin • Client is obese
• Client is prone to • Client is prone to
diabetic hyperglycemic,
ketoacidosis (DKA) hyperosmolar non- Clinical Manifestations:
ketotic coma (HHNC) • Polyuria, Polydipsia, Polyphagia
• -
Weight gain/ loss Blurred vision
type ! Slow wound healing
• Infections: pyorrhea (periodontal infections),
urinary tract infections, vasculitis, cellulitis,
furuncles, carbuncles, vaginal infections
• Weakness and paresthesia, signs of
inadequate circulation in the feet
• Signs of accelerated atherosclerosis (renal,
cerebral, cardiac, peripheral)

Laboratory and Diagnostic Procedures

• Fasting blood glucose level above 140 mg/dl
or postprandial blood glucose level above
200 mg/dl measured on more than one
occasion is diagnostic
• Glycosylated hemoglobin reveals elevated
blood glucose level over the previous 2 to 4
months
• Glucose tolerance test reveals blood glucose
over 200 mg/dl at the 2-hr sample
Nursing Management • The peak of action time of insulin is
1. Diet: Low caloric diet, 20% CHON, 30% important because of the possibility of
fats, 50% CHO, High fiber diet. Complex hypoglycemic reactions occurring that time.
carbohydrates like rice, bread, pasta, root • Types of Insulin
crops are preferred over simple o Rapid-acting insulin (Lispro, Aspart)
carbohydrates like cakes, pastries. o Short-acting insulin (Regular,
2. Activity and Exercise increases CHO uptake Humulin R)
by the cells, decreases insulin requirements. o Intermediate-acting insulin (NPH)
Instruct client on dietary adjustments when o Long-acting insulin (Glargine,
exercising. Instruct client to monitor blood Ultralente)
glucose levels before, during and after o Premixed insulin (Humulin 70/30)
exercise. If blood glucose level is greater than o Know the onset, peak and duration.
250 mg/dl and urinary ketones are present, • Insulin administration
instruct client not to exercise until blood 1. Route: SQ promotes slower
glucose is normal and urinary ketones are absorption, less painful; IV during
absent. DKA emergency
2. Sites of insulin injections: abdomen,
Medical Management arms (posterior surface), thigh
Oral hypoglycemic agents stimulate islets of (anterior surface), buttocks
Langerhans to secrete insulin, increase sensitivity of 3. Administer insulin at 90 degrees.
peripheral receptors to insulin, decrease hepatic Most insulin syringe have needle
glucose output or delay intestinal absorption of gauge 27 to 29, 1⁄2 inch long. Do not
glucose, thus decreasing serum glucose levels. massage injection site to prevent
Indicated only in Type II DM. rapid absorption.
• Sulfonylureas- oldest class of OHA; 4. Injections should be 1⁄2 inch apart
stimulate the pancreas to produce more within the anatomical area. Finish all
insulin (Glipizide, glimepiride) sites in one anatomical area before
• Biguanides lower blood glucose levels going to another area.
without stimulating insulin secretion 5. Lipodystrophy inhibits insulin
(Metformin) absorption. To prevent lipodystrophy
• Thiazolidineione- reduces insulin resistance (hard fatty masses in subcutaneous
(Pioglitazone) layers):
• Alpha-glucosidase inhibitors hamper the a. Systematic rotation of the site
digestive enzyme that breaks carbohydrates of injection. Reuse one site
into smaller sugar (Acarbose) after at least 2 to 3 weeks.
• Meglitinides stimulate insulin secretion by b. Administer insulin at room
the pancreas (Nateglinide, Repaglinide) temperature.
6. If a vial of insulin will be used up in
Insulin therapy 30 days (1 month), it may be kept at
• Indicated in Type I DM and in Type II DM room temperature. Otherwise, the vial
when diet and weight control are ineffective should be refrigerated.
to maintain blood glucose levels. 7. Avoid exposing insulin to extremes of
• Regular insulin is the only insulin that can temperature.
be administered intravenously in the 8. Regular insulin maybe mixed with
emergency treatment of diabetic any other type of insulin. Insulin zinc
ketoacidosis. suspensions (intermediate-acting)
• Illness, infection and stress can elevate blood may be mixed only with each other
glucose levels and the need for insulin. and regular insulin.
Insulin should not be withheld during illness, 9. To mix insulin, draw up the regular
infection or stress because hyperglycemia insulin first.
and ketoacidosis can result.
 10. Administer a mixed dose of insulin • Acute complications:
within 5 to 15 minutes of preparation. o Hypoglycemia Hyperglycemia
After this time, the regular insulin o Diabetic Ketoacidosis (DKA)
binds with the NPH insulin and its o Hyperglycemic Hyperosmolar
action is reduced Nonketotic Syndrome
• Complications of Insulin Therapy
o Local allergic reactions- redness, HYPOGLYCEMIA
swelling, tenderness and induration or • Occurs when blood glucose level falls below
wheal at the site of injection may 60 mg/dl
occur 1-2 hrs after administration.
o Insulin Lipodystrophy Causes:
§ Lipoatrophy is the loss of 1. Overdose of insulin or OHA
subcutaneous fat and appears 2. Omission of meals or little food
as slight dimpling. The use of 3. Strenuous exercise or excessive activity
human insulin helps prevent 4. Gastrointestinal upset (i.e. nausea, vomiting,
this complication. diarrhea)
§ Lipohypertophy is the
development of fibrous fatty Classifications of Hypoglycemia
masses at the injection site • Mild hypoglycemia- blood glucose level less
and is caused by repeated use than 60 mg/dl. Hunger, nervousness,
of an injection site. palpitations, sweating, tachycardia, tremors
o Insulin Resistance- lack of tissue • Moderate hypolgycemia- blood glucose
sensitivity to insulin from the body, level less than 40 mg/dl. S/Sx: Confusion,
which results in hyperglycemia. May double vision, drowsiness, emotional
be managed by administering a purer changes, headache, impaired coordination,
insulin. inability to concentrate, irrational or
• Complications of Insulin Therapy combative behavior, light headedness,
o Dawn Phenomenon- results from the memory lapses, numbness of lips and tongue,
reduced tissue sensitivity to insulin slurred speech
that develops 5 to 8 am (pre-breakfast • Severe hypoglycemia- blood glucose level
hyperglycemia). Treatment is less than 20 mg/dl. S/Sx: Inability to
administering NPH insulin at 10PM. swallow, loss of consciousness, seizures
o Somogyi Phenomenon- normal or
elevated blood glucose levels are Signs and Symptoms:
present at bedtime. Hypoglycemia • Shaky
occurs at 2 to 3 AM , which triggers • Fast heartbeat (tachycardia)
production of counterregulatory • Sweating/ diaphoresis
hormones (epinephrine,
• Dizzy
norepinephrine and glucocorticoid).
• Anxious
By 7 AM, in response to these
hormones, the blood glucose • Hungry
rebounds to hyperglycemic range. • Blurry vision
Treatment for this phenomenon • Weakness or fatigue
included decreasing the evening dose • Headache
of NPH or increasing bedtime snack. • Irritable
o Insulin Waning- Progressive rise in
blood glucose level from bedtime to Nursing Management
morning. Treatment includes 1. Mild hypoglycemia- Give 10-15 grams of
increasing the evening dose of NPH fast-acting simple carbohydrates. (i.e.
or long-acting insulin before the Commercially prepared glucose tablets, 6-10
evening meal if one is not already Life Savers or hard candy, 4 tsp sugar, 1 tbs
prescribed.
 of honey or syrup, 1⁄2 cup of fruit juice or mg/dl. To prevent abrupt fall of blood
soda, 8 oz low fat milk., 3 graham crackers). glucose.
2. Moderate hypoglycemia- Give 15 to 30 4. Treat hyperglycemia with regular insulin IV
grams of fast-acting simple carbohydrates. bolus followed by continuous infusion, as
3. Severe hypoglycemia- If unconscious or prescribed.
unable to swallow, administer Glucagon SQ, 5. Monitor potassium levels, glucose levels and
IM or IV. A second dose if the client remains urinary output and for signs of increased
unconscious. Glucagon is used to treat intracranial pressure (ICP).
insulin-induced hypoglycemia. Administer
50% dextrose in water, 25 to 50 ml, IV as HYPERGLYCEMIC HYPEROSOMOLAR
prescribed. NONKETOTIC SYNDROME
• Severe hyperglycemia that occurs without
DIABETIC KETOACIDOSIS ketosis and acidosis.
A life-threatening complication of type I DM due to • Occurs in type II DM.
severe insulin deficiency.
Causes: Clinical Manifestations:
1. Underdose or missed dose of insulin • Hyperglycemia- blood glucose level 600 to
2. Illness of infection 2,000 mg/dl Hypotension, dehydration,
3. Overeating tachycardia
4. Stress, surgery • Mental status changes, neurologic deficits,
5. Undiagnosed and untreated type I DM seizures

Pathophysiologic Mechanisms -O
Management:
1. Hyperglycemia- blood glucose levels range • Treatment is similar to DKA
from 300 to 800 mg/dl. • Fluid replacement
2. Dehydration and electrolyte loss
• Electrolyte correction
3. Acidosis- low serum bicarbonate and low pH
• Insulin administration
Clinical Manifestations:
Chronic Complications of DM
• Acetone breath Diabetic retinopathy- chronic and progressive
(fruity odor)
impairment of the retinal circulation that eventually
• Anorexia, nausea, causes hemorrhage. Permanent blindness can
vomiting, occur.
abdominal pain
• Headache Clinical Manifestations:
• Hypotension • Rupture of microaneurysms in retinal blood
Kussmaul’s vessels causes changes in vision, blurred
respirations Mental vision due to macular damage
status changes • Sudden loss of vision due to retinal
Polydipsia detachment, Cataract from lens opacity
• Polyuria
• Weak, rapid pulse Management
• Weakness 1. Control hypertension and blood glucose
levels.
Nursing Management 2. Laser therapy to remove hemorrhagic tissue
1. Maintain paten airway. Administer oxygen. to decrease scarring
2. Treat dehydration with normal saline 0.9% or 3. Vitrectomy to remove vitreous hemorrhage
0.45% rapid IV as prescribed. and prevent retinal detachment
3. D5NSS or 5% dextrose in 0.45% saline when 4. Cataract removal
the blood glucose level reaches 250 to 300
Diabetic nephropathy comfortable, properly fitted pair of shoes
• Progressive loss of kidney function. ·

(leather is preferred).
8. Do not wear open-toed shoes or shoes with
Clinical Manifestations: strap that goes between the toes.
• Microalbuminuria, Thirst, Fatigue, Anemia, 9. Do not wear the same pair of shoes two days
Weight loss, malnutrition, Frequent urinary in a row.
tract infection 10. Check shoes for cracks or tears in the lining
and for foreign objects before putting them
Management: on. Do not go barefooted.
1. Control of hypertension and blood glucose 11. Avoid self-treatment of corns, blisters or
levels. ingrown. Consult podiatrist.
2. Monitor VS, intake and output, serum BUN
and creatinine, urine albumin.
3. Restrict dietary protein, sodium and
potassium intake.
4. Prepare client for dialysis, kidney transplant
or pancreas transplant as prescribed.

Diabetic neuropathy
• General deterioration of the nervous system.
• Complications include non-healing foot
ulcers, gastroparesis (affects the normal
spontaneous movement of the muscles
(motility) of the stomach) or erectile
dysfunction

Clinical Manifestations: DISORDERS OF THE ADRENAL GLANDS

• Paresthesia, Decreased or absent reflexes, • Hypofunction: Addison’s Disease
diminished sensation, Pain, aching and • Hyperfunction: Cushing’s Syndrome and
burning in the lower extremities, Diminished Conn’s Disease
peripheral pulses, Skin breakdown and signs
of infection, Dizziness, postural hypotension, ADDISON’S DISEASE > most - common
form of

Diarrhea, constipation, Incontinence, •

advenal
Hyposecretion of adrenal cortex hormones hypofunction
Dyspareunia, Impotence (3S)
• Hypoglycemic unawareness
Etiology:
Nursing Management • Autoimmune disorders
1. Control of hypertension and blood glucose • Tuberculosis
levels. • Fungal disease
2. Administer pain medications as prescribed.
3. Initiate bladder training program (for “Everything is low and slow except potassium”
neurogenic bladder).
4. Use of estrogen-containing lubricant for Clinical Manifestations:
dyspareunia. • Weakness
5. Penile injection or implantable devices as • Weight Loss
prescribed
• Hypoglycemia
6. Foot care to prevent trauma and gangrene
• GI Disturbances
formation.
7. Inspect the feet daily. Wash the feet with • Postural Hypotension
warm water and mild soap. Pat dry. Wear • Bronze Pigmentation of Skin
• Changes In Distribution of Body Hair
Adrenal Crisis: and high carbohydrate provides nutritional
• Profound Fatigue support to prevent muscle wasting. High
• Dehydration potassium diet prevents hypokalemia. Low
• Vascular Collapse (Low Blood Pressure) sodium prevents hypernatremia and retention
• Renal Shut Down of water.
• Low Serum NA 8. Contraindications of corticosteroids
• High Serum K • Corticosteroids are contraindicated in
psychosis and fungal infections.
1. Note the generalized skin pigmentation (in a • Should be used in caution win clients
Caucasian patient) but especially the with DM, hyperglycemia may occur.
deposition in the palmer skin creases, nails • Dexamethasone decreases the effects
and gums. of coumadin and oral hypoglycemic
Nursing Management agents.
1. Monitor VS especially BP, weight, intake and • Corticosteroids when used with
output. aspirin and NSAIDs increase the risk
2. Monitor blood glucose and serum potassium of GI bleeding and ulceration.
levels. • Use of potassium wasting diuretics
3. Administer glucocorticoid or increases potassium loss resulting to
mineralocorticoid medications as prescribed: hypokalemia.
• Celestone (Betamethasone) • Advise the client to wear Medic-Alert
• Cortone, Cortistan (Cortisone) bracelet.
• Decadron (Dexamethasone) 9. Dose should be tapered and not stopped
• Florinef (Fludrocortisone) abruptly. To prevent Addisonian crisis,
• Cortef (Hydrocortisone) weakness, psychologic letdown.
• Medrol, Depo-Medrol, Solu-Medrol 10. Monitor for side effects.
(Methylprednisolone)
CUSHING’S SYNDROME > cluster physicalnormalities
• Delta- cortef, Prelone, Orapred,
-

Adrenal hyperfunction, also known as Cushing’s

Pediapred (Prednisone)
syndrome, involves excessive production of
• Aristocort, Kenacort (Triamcinolone)
adrenocortical hormones, primarily cortisol, but
also androgens and mineralocorticoids. The
Hormonal Replacement Therapy
incidence is higher among women than men.
1. Monitor VS. Sodium and water retention may
cause elevation of BP.
Etiology
2. Monitor weight, intake and output for edema.
1. The most common cause is bilateral adrenal
3. Monitor serum potassium and calcium levels.
hyperplasia
Steroids may cause hypokalemia and
2. Adrenal adenomas and carcinomas
hypocalcemia.
3. Tumors in other organs such as lungs and
4. Avoid exposure to infections. Steroids may
pancreas that produce ectopic ACTH
mask the signs of infection and are
4. Prolonged steroid therapy
immunosuppressants.
5. Administer steroids after meals or with milk.
Clinical Manifestations:
Steroids stimulate gastric acid secretions and
• Personality changes
may cause gastric irritation and peptic ulcer
disease. • Hyperglycemia
6. Monitor urine and blood glucose levels and • CNS irritability
urine ketones. Breakdown of fats and • Na and fluid retention
proteins causes hyperglycemia and formation • GI distress and increased acid
of ketones. • Moon face
7. Diet should be high in protein, high • Increased susceptibility to infection
carbohydrate, high potassium, low sodium. • Males: gynecomastia
Steroids enhance metabolism. High protein • Females: amenorrhea and hirsutism
 • Osteoporosis
• Thin skin
• Purple striae
• Bruises and petechiae
• Thin extremities

CONN’S DISEASE (Hyperaldosteronism)

• Hypersecretion of aldosterone from the
adrenal cortex.
• Most common cause is adenoma.

Signs and Symptoms:

• Hypertension, Hypokalemia, Polydipsia,
Polyuria, Hypernatremia

Nursing Management
1. Monitor vital signs, serum potassium, intake
and output and urine
2. Administer Spironolactone (Aldactone), a
potassium-sparing diuretic and aldosterone
antagonist.
3. Administer antihypertensives, as prescribed.
4. Prepare client for adrenalectomy.
5. Instruct client on glucocorticoid therapy
following adrenalectomy.
Lifelong glucocorticoid replacement therapy
is necessary for bilateral adrenalectomy.
Temporary glucocorticoid replacement up to
2 years is necessary for a unilateral
adrenalectomy.
·

trasphenoidal

D hyperaldesteronism

2
·

D Pheocomocytoma

T
 FAR EASTERN UNIVERSITY
Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Module 3Care of Clients with Neurologic Alterations

OUTLINE 3. Processes the information in the brain and

1. Anatomy and Physiology of the Nervous spine – Integration Function
System 4. Sends information to the muscles, glands, and
2. Neurological System Assessment organs so they can respond appropriately –
3. Management of the Unconscious Neurologic Motor Function
Client
4. Increased Intracranial Pressure It controls and coordinates all essential functions of
5. Management of Client Undergoing the body including all other body systems allowing
Neurological Procedures the body to maintain homeostasis or its delicate
6. Paroxysmal Disorders balance.
7. Cerebral Blood Circulation
8. Cerebrovascular Accident (Stroke) DIVISIONS OF THE NEVOUS SYSTEM
a. Ischemic Stroke • Central Nervous System (CNS) and
b. Hemorrhagic Stroke the Peripheral Nervous System (PNS)
9. Intracranial Aneurysm
10. Neurologic Trauma
a. Cranio Cerebral Trauma
b. Scalp Injury
c. Skull Fractures
11. Brain Injury
a. Focal Brain Injuries
b. Diffused Head Trauma
12. Spinal Cord Injuries
13. Inflammatory Neurologic Diseases
a. Brain Abscess
b. Meningitis
14. Neurologic Degenerative Disorders
a. Multiple Sclerosis
b. Ring or Donut Scotoma
c. Parkinson’s Disease
d. Amyotrophic Lateral Sclerosis (Lou
Gehrig’s Disease)
e. Myasthenia Gravis NEURON
f. Huntington’s Disease • Basic functional cell of nervous system
15. Cranial Nerve Disorders • Transmits impulses (up to 250 mph)
a. Trigeminal Neuralgia
b. Bell’s Palsy Parts of a Neuron
• Dendrite – receive stimulus and carries it
THE NERVOUS SYSTEM impulses toward the cell body
FUNCTIONS OF THE NERVOUS SYSTEM • Cell Body with nucleus – nucleus & most of
1. Gathers information from both inside and cytoplasm
outside the body - Sensory Function • Axon – fiber which carries impulses away
2. Transmits information to the processing areas from cell body
of the brain and spine • Schwann Cells- cells which produce myelin
or fat layer in the Peripheral Nervous System
 • Myelin sheath – dense lipid layer which • Diencephalon – thalamus & hypothalamus
insulates the axon – makes the axon look gray • Cerebellem
• Node of Ranvier – gaps or nodes in the • Cerebrum
myelin sheath Spine
• Impulses travel from dendrite to cell body • Spinal Cord
to axon
Meninges
Three types of Neurons Meninges are the three coverings around the brain
• Sensory neurons – bring messages to CNS & spine and help cushion, protect, and nourish the
• Motor neurons - carry messages from CNS brain and spinal cord.
• Interneurons – between sensory & motor • dura mater is the most outer layer, very tough
neurons in the CNS • arachnoid mater is the middle layer and
adheres to the dura mater and has web-like
Impulses attachments to the innermost layer, the pia
• A stimulus is a change in the environment mater
with sufficient strength to initiate a response. • pia mater is very thin, transparent, but tough,
• Excitability is the ability of a neuron to and covers the entire brain, following it into
respond to the stimulus and convert it into a all its crevices (sulci) and spinal cord
nerve impulse • cerebrospinal fluid, which buffers, nourishes,
• All of Nothing Rule – The stimulus is either and detoxifies the brain and spinal cord,
strong enough to start and impulse or nothing flows through the subarachnoid space,
happens between the arachnoid mater and the pia
• Impulses are always the same strength mater
along a given neuron and they are self-
propagation – once it starts it continues to REGIONS OF THE BRAIN
the end of the neuron in only one
direction- from dendrite to cell body to
axon
• The nerve impulse causes a movement of
ions across the cell membrane of the nerve
cell.

Synapse
• Synapse - small gap or space between the
axon of one neuron and the dendrite of
another - the neurons do not actually tough
at the synapse
• It is junction between neurons which uses • Cerebellum – coordination of movement
neurotransmitters to start the impulse in the and aspects of motor learning
second neuron or an effector (muscle or • Cerebrum – conscious activity including
gland) perception, emotion, thought, and planning
• The synapse insures one-way transmission of • Thalamus – Brain’s switchboard – filters
impulses and then relays information to various brain
regions
Neurotransmitters • Medulla – vital reflexes as heart beat and
Neurotransmitters – Chemicals in the junction respiration
which allow impulses to be started in the second • Brainstem – medulla, pons, and midbrain
neuron (involuntary responses) and relays
information from spine to upper brain
CENTRAL NERVOUS SYSTEM • Hypothalamus– involved in regulating
Brain activities internal organs, monitoring
• Brain stem – medulla, pons, midbrain information from the autonomic nervous
 system, controlling the pituitary gland and its o Parasympathetic nervous system –
hormones, and regulating sleep and appetite. when body is at rest or with normal
functions
LOBES OF THE CEREBRUM § Normal everyday conditions
• Frontal – motor area involved in
movement and in planning &
coordinating behavior
• Parietal – sensory processing, attention,
and language
• Temporal – auditory perception,
speech, and complex visual perceptions
• Occipital – visual center – plays a role
in processing visual information

ASSESSMENT OF NEUROLOGICAL
SYSTEM
MAIN COMPONENT OF NEUROLOGIC
EXAM
COMPREHENSIVE NEUROLOGIC HISTORY
Establishing a Nursing Database
1. History Taking
a. Health History
PERIPHERAL NERVOUS SYSTEM b. Family History
Cranial nerves c. Past and present neuro health history
• 12 pair d. Activity of Daily Living
• Attached to undersurface of brain
INTERVIEW
Spinal nerves The patient/family interview will allow the nurse to:
• 31 pair 1. Gather data: both subjective and objective
• Attached to spinal cord about the patient's previous/present health
state
SOMATIC NERVOUS SYSTEM (Voluntary) 2. Provide information to patient/family
1. Relays information from skin, sense organs 3. Clarify information
& skeletal muscles to CNS 4. Make appropriate referrals
2. Brings responses back to skeletal muscles 5. Develop a good working relationship with
for voluntary responses both the patient and the family
6. Initiate the development of a written plan of
AUTONOMIC NERVOUS SYSTEM care which is patient specific
(Involuntary)
• Regulates bodies involuntary responses Interview to identify presence of:
• Relays information to internal organs 1. headache
• Two divisions 2. difficulty with speech
o Sympathetic nervous system – in 3. inability to read or write
times of stress 4. alteration in memory
§ Emergency response 5. altered consciousness
§ Fight or flight 6. confusion or change in thinking
7. disorientation
8. decrease in sensation, tingling or pain
 9. motor weakness or decreased strength Akinetic Mutism- state of unresponsiveness to the
10. decreased sense of smell or taste environment in which no movement or sounds is
11. change in vision or diplopia being initiated by the client, but eyes open at a time
12. difficulty with swallowing
13. decreased hearing Persistent Vegetative State
14. altered gait or balance • Patients in this state have no thinking abilities
15. dizziness or awareness of their surroundings.
16. tremors, twitches or increased tone • They do, however, retain non-cognitive
function and normal sleep patterns.
NEUROLOGIC PHYSICAL EXAMINATION • Although those in a persistent vegetative state
1. Mental Status Assessment lose these higher brain functions, others, such
2. Cranial nerve Assessment as breathing and circulation, remain intact.
3. Motor Function Assessment • Spontaneous movement may occur and the
4. Muscle Strength Assessment eyes may open in response to stimuli.
5. Assessment of movement, posture, gait • Individuals in a persistent vegetative state
6. Assessment of cerebellar function may appear normal, but they cannot speak or
7. Neuro Vital Sign Assessment and Clinical respond to commands.
Implication
8. Pupillary Response and sizes CAUSES OF UNCONSCIOUSNESS
9. Glasgow Coma Scale • Neurologic (head injury Toxicologic (drug
1. Best Eye Response overdose, alcohol intoxication)
2. Best verbal Response
• Metabolic (hepatic or renal failure, diabetics
3. Best Motor Response ketoacidosis)
10. Identifying Level of Consciousness
1. Conscious COMMON DRUGS USED FOR CLIENT
2. Confusion
WITH ALTERED NEUROLOGIC
3. lethargic FUNCTIONS
4. Obtundation 1. Phenobarbitals
5. Stupor 2. Hydantoins
6. Coma 3. Benzodiazepines
a. Light coma 4. Carbamazepine
b. Deep coma 5. Phenytoins
11. Deep Tendon Reflexes, gag and coughing 6. Valproic Acid
reflexes 7. Furosemide
a. Caloric Reflex Test 8. Mannitol
b. Oculovestibular Reflex Test 9. SumaTriptan
10. DihydroErgotamine
MANAGEMENT OF THE UNCONSCIOUS 11. Acetaminophen
NEUROLOGIC CLIENT & ALTERED 12. Lactulose
NEUROLOGIC ASSESSMENT 13. Thorazine
Unconsciousness – it is a condition in which the 14. Demerol
client is unresponsive to and unaware of 15. Propofol
environmental stimuli, usually for a short duration 16. Dexamethasone
17. Dantrolene (Dantrium)
TYPES OF UNCONSCIOUSNESS 18. Penicillin
Coma- clinical state of unconsciousness in which the 19. Ceftrioxone Na
client exhibits unawareness of self or the 20. Prostigmine
environment for prolonged periods (day to 21. Corticosteroid(prednisone)
even years) 22. Riluzole
23. Neurontin
24. Quinine
 25. Levodopa
26. Symmetrel
27. Dopamine HCl
28. Dobutamine HCl
29. Citicholine
30. Nicardipine
31. Vit. B complex
32. Nimodipine
33. Aspirin

INCREASED INTRACRANIAL PRESSURE

Definition: The skull is a hard, bony vault filled with
brain tissue, blood and cerebrospinal fluid (CSF). A
balance between these: 3 components maintain the
pressure within the cranium.
1. The Brain 84%
2. The blood 4%
3. CSF 12% CUSHING’S TRIAD
Cushing Triads- suggests a cerebral hemorrhage in
Normal range of ICP : 5-15 mmHg the setting of trauma or an space occupying lesion
(e.g. brain tumor) that is growing and a possible
CEREBRAL RESPONSE TO INCREASED ICP impending fatal herniation of the brain.
MONRO-KELLIE HYPOTHESIS: 1. Hypertension (progressively increasing
A theory for understanding ICP states that because systolic blood pressure)
the bony skull cannot expand when one of the three 2. Bradycardia
components expands, the other two must compensate 3. Widening pulse pressure (an increase in the
by decreasing in volume for the total brain volume difference between systolic and diastolic
and pressure to remain constant. pressure over time)
4. Herniation The brain Shift from the
compartment greater pressure to a
compartment of lesser pressure

MANAGEMENT OF CLIENT UNDERGOING

NEUROSURGICAL PROCEDURES
The pre and intraoperative nursing management
1. Positioning
2. procedures and other therapeutic
management

Post-Operative Nursing management

1. Prevention of complication
o Brain stem herniation
o Irreversible brain anorexia and brain
death
o Diabetes insipidus & Syndrome of
Inappropriate Antidiuretic Hormone
(SIADH)
2. Common neurologic deficits in post-
operative period
3. Nursing responsibilities
 o ICP monitoring: ICP monitoring is • These can be unpredictable and lead to falls
most often used in head trauma in the and subsequent injuries.
following situations:
1. GCS less than 8 CAUSES:
2. Drowsy with CT findings • Head Trauma
(operative or non-operative) • Alcohol withdrawal
3. Post op hematoma evacuation • Brain Tumor
4. High risk patients • Idiopathic
o Above 40 yrs.
• Metabolic disorders
o Low BP
o those who requires ventilation SIGNS AND SYMPTOMS:
• Twitching muscles
Medical and/or Surgical Management:
• Convulsive movement
• H – Head elevated to 30degrees to promote
venous drainage & respiratory. • Tingling sensation
• E – Evaluate neurologic status (ICP). • Sweating
• A – Airway. Evaluate current respiratory • The perception of an unusual smell or taste
pattern. • Hallucination
• D – DRAINAGE – drainage from the ears • Fear or Anxiety
may be Cerebral Spinal Fluid • Changes in awareness
• Loss of consciousness
Nursing Care: Apply a sterile dressing over ear and • Other changes:
evaluate for Signs of meningitis o A person who has a psychic
manifestation, a person may
• S – Seizure Precautions. experience an aura like strange smell,
• M - Monitor ICP noise or a sense of rising or welling
• - Osmotic diuretics up in the epigastric region and “déjà
• R - Reduce CSF and blood volume by vu” in which unfamiliar surroundings
draining CSF via vetriculostomy drain. inexplicably seem familiar to

Nursing Diagnoses MANAGEMENT:

1. Ineffective airway clearance r/t accumulation • Depending on the specific condition, some of
of secretion these disorders are treated with bedside care
2. Ineffective cerebral perfusion r/t effects of while others require further management and
increase ICP treatment with medications.
3. Risk for fluid volume deficit r/t dehydration • In some cases, rehabilitation is indicated to
4. Risk for infection r/t ICP monitoring system develop compensatory strategies to enable
5. Ineffective breathing pattern r/t neurologic one to return to their previous level of
dysfunction ( brain stem dysfunction) function before the onset of their problem.

PAROXYSMAL DISORDER CEREBRAL BLOOD CIRCULATION

Paroxysmal Disorder is an excessive discharge of Cerebral blood circulation refers to the movement
electrical activity within the brain, which leads to a of blood through the network of blood vessels
change in movement, sensation, experience or supplying the brain.
consciousness. These are disorders that occur
unexpectedly.
Two Networks of Blood Vessels Supplying the
EXAMPLES OF THIS INCLUDE: Brain
• intermittent room spinning dizziness 1. Arteries: deliver oxygenated blood, glucose
• intermittent swaying sensations and other nutrients to the brain
• collapses and seizures.
 2. Veins: carry deoxygenated blood back to the and consciousness), and the hypothalamus
heart, remo ving CO2, lactic acid and other (regulating metabolism and the release of hormones,
metabolic products. among other functions).Through its branches, this
artery also delivers blood to the eyes and their related
structures, the forehead, as well as the nose.

The vertebral artery delivers blood to the neck’s

vertebrae, upper spinal column, the space around the
outside of the skull. It also supplies blood to two very
important regions of the brain: the posterior fossa and
the occipital lobes.

The posterior fossa is the small space in the skull

near the brain stem and cerebellum, which are
associated with essential functions like breathing and
keeping in balance. The occipital lobes are essential
for visual processing and house the primary visual
cortex.
The anterior circulation is the blood supply to the
anterior portion of the brain, including most of the CEREBROVASCULAR ACCIDENT
supratentorial structures excluding the occipital (STROKE)
lobes. The anterior circulation is supplied by the Stroke is a term used to describe neurologic changes
internal carotid arteries which each divide into two caused by an interruption in blood supply to a part of
the large terminal branches, the anterior cerebral and the brain. CVA results in cerebral anoxia and
middle cerebral arteries. Due to the anastomotic impaired cerebral metabolism, which damages
circle of Willis, the anterior circulation connects via brain tissues. CVA results from occlusion of the
the posterior communicating arteries to the posterior intracranial or extracranial artery, commonly
circulation. associated with atherosclerotic plaque.
The posterior cerebral circulation (or simply, Cerebrovascular disorders (CVA) is the third leading
posterior circulation) is the blood supply to the cause of death in the United States and account for
posterior portion of the brain, including the occipital about 167,000mortalities annually.
lobes, cerebellum and brainstem. Due to the
anastomotic circle of Willis, the posterior circulation RISK FACTORS
connects via the posterior communicating arteries to 1. Age
the anterior circulation. The posterior circulation is 2. Sex
supplied by the vertebral arteries that combine to 3. Heart Diseases
form the basilar artery which then divides into the 4. High cholesterol level
posterior cerebral arteries. From these main vessels, 5. DM
many smaller vessels supply the posterior structures 6. Cigarette smoking
of the brain, including: 7. Prior stroke events
• posterior inferior cerebellar artery
• anterior inferior cerebellar artery COMMON SITES
• pontine branches • Middle Cerebral Artery– hemiparesis
• superior cerebellar artery. • Internal carotid Artery– hemiplegia
• Right hemispheric lesion– spatial
The primary role of the internal carotid artery is to disorientation
deliver blood to the forebrain: the front part of the • Left Hemispheric lesion– language
brain that houses the cerebral hemispheres (which disturbance
are involved higher-level cognition, language, as
well as visual processing), the thalamus (associated
with visual, sensory, and auditory processing, sleep,
 CLINICAL MANIFESTATIONS CINCINNATI PREHOSPITAL STROKE
Early Warnings SCREENING
• Transient Hemiparesis 1. Check for facial drooping have patient smile or
• Loss of speech show teeth.
• Hemisensory Loss 2. Check for arm drift by having patient close
eyes and hold arms out for 10seconds
Neurological Deficits Motor Visual 3. Evaluate the patient’s speech. Have the Patient
• Hemiparesis- weakness of one side of the say a phrase to see if there is any abnormal
body or part of it speech pattern. Such as: “The Sky is Blue in
• Diplopia– double vision Cincinnati.”
• Hemiplegia–paralysis of one side of the body
or part of it Interpretations:
• Homonymous Hemianopsia– blindness in • Patients with one of these 3 findings-as anew
half of the visual field in one or both eyes event-have a 72% probability of an ischemic
• Dysphagia- difficulty in swallowing stroke
• Dysarthria-difficulty in speaking • If all 3 findings are present, the probability of
an acute stroke is more than 85%.
Verbal Cognitive
TERMS TO DESCRIBE MOTOR
• Aphasia–inability to communicate
DYSFUNCTION
o Expressive Aphasia- inability to
express one self • -plegia: means stroke or paralysis
o Receptive Aphasia- inability to • -paralysis: means loss of movement
understand language • -paresis: means weakness
o Global Aphasia (mixed)- Affects • -mono: one limb
both comprehension & speech • -hemi: both limbs on one side
production • -di or para: both upper limbs or both lower
• Poor abstraction/Amnesia– form of memory limbs
loss • -quadri-or tetra: all four limbs

DIAGNOSTIC TESTS NURSING DIAGNOSES FOR CVA

Initial Studies: • Impaired verbal Communication
• CT scan • Unilateral neglect r/t perceptual Disruption
• MRI • Impaired swallowing r/t neuromuscular
impairment
Supportive Studies • Disturbed body image r/t actual change in
• Cerebral Angiography body structure, function & appearance
• Carotid Ultrasound-PET scan • Deficit knowledge: Discharge regimen r/t
• Transcranial Doppler Flow Studies lack of previous exposure to information

OUTCOME MANAGEMENT MEDICAL AND PHARMACOLOGIC

• Early Detection: MANAGEMENT
o Glasgow Coma Scale • Surgical clipping or ligation of aneurysm and
o National Institutes of Health Stroke evacuation of blood.
Scale • Administration of calcium channel blocker
o Acute Stroke QuickScale (NIMODIPINE)
• Maintain Cerebral Oxygenation • Neuroradiology, CSF drainage
o Mechanical ventilation • Mannitol
• Optimum O2-Airway patency • Prevent acute systemic HPM (maintain
systolic BP to 150mmHg and administer
hypertensive drugs.
 • Atherosclerotic Vertebral or Basilar
plaque at large Arteries
NURSING RESPONSIBILITIES vessel of the Posterior Cerebral
• Nimodipine (Nimotop)- Produces selective brain Artery
blockade of calcium channels cerebral blood • Develops during Anterior Cerebral
sleep or withing Artery
flow. hour of arising
o Nimodipine is the ONLY Cardiogenic Moving clot or Affects temperature
APPROVED Emboli Stroke thrombus from the regulation (hypo or
left heart travels to hyperthermia)
o Instruct client to swallow sustained the brain à lodged Affects urinary
release formulations whole without in the smaller blood output
crushing or chewing vessels à
narrowing of the
o Prevents cerebral arterial spasm that lumen à occlusion
follows subarachnoid Hemorrhage à decreased O2
that can result to neurologic deficit. supply
o Dosing ( 60mg every 4hrs) should be Small Vessel Occlusion of the Aphasia, visual
Stroke (lacunar smaller branches of changes, attention
given within 96hrs of SAH and stroke) large cerebral deficit, and altered
continue for 21 days. arteries caused by LOC
o MUST NOT be given parenterally HPN
(e.g. IM or IV) owing to a risk of
potentially fatal cardiovascular Thrombotic Stroke
Artery Location S/Sx
events. Involvement
Anterior Infection of the Paralysis of the
MAJOR TYPES OF STROKES Cerebral frontal lobe contralateral foot
Artery Impaired gait
ISCHEMIC STROKE Problem in decision
Ischemic-are caused by a thrombotic or embolic making
blockage of blood flow to the brain. It account for Aphasia
Urinary incontinence
about 83% of all strokes Middle Massive infection of Hemiplegia
Cerebral lateral hemisphere Aphasia
• Most common cause: thromboembolism Artery and deeper structure Hemianopsia
of frontal, parietal, Altered LOC
• Possible sources of clot: temporal, and basal Confusion
• Heart- Large artery (to brain) ganglia
Posterior Occipital lobe Color blindness
• Small artery in brain Cerebral Anterior and medial Loss of central vision
Artery portion of temporal Visual hallucination
Types of Ischemic Stroke lobe Memory deficit
Type of Ischemic Pathophysiology S/Sx Basilar Artery Cerebellum and Diplopia, dysphagia
Stroke brain stem Dysphonia, amnesia
Transient Microemboli Sensory: receptive Weakness on affected
Ischemic Attack released from the aphasia/ impaired side
(TIA) thrombus which comprehension
impede blood flow Motor: expressive; HEMORRHAGIC STROKE
• Little or minimal disruption to
strokes produce speech Hemorrhagic- caused by bleeding into the brain
• Symptoms Acoustic: difficulty tissue or the subarachnoid space. The remaining 17%
usually last 24- of comprehending of strokes are hemorrhagic.
72 hours then speech
resolve Visual A: loss of
• Precursor to a ability to Subarachnoid Hemorrhage
CVA within 2 comprehend visual • Most common cause: aneurysm rupture
yes of onset of symbols resulting to
TIA difficulty in reading • Other causes: Vessel malformation, tumor,
Ischemic Presence of dying Edema, increased bleeding abnormalities
Penumbra cells in the ICP
involving stroke
Large Vessel Atherosclerotic Internal carotid
Stroke blood vessels artery (Hemiplegia)
(Thrombotic) • Narrowing of the Middle Cerebral
lumen of the artery
artery
Types of Hemorrhagic Stroke 1. Internal carotid artery
Types of Pathophysiology S/Sx 2. Anterior cerebral artery
hemorrhagic
stroke
3. Anterior communicating artery
Thalamic Rupture of the blood Hemiplegia 4. Posterior communicating artery
stroke vessels à bleeding into Aphasia 5. Posterior cerebral artery
the brain tissue à
edema, compression of
6. Middle cerebral artery.
the brain content
SIGNS & SYMPTOMS
Cerebral hemorrhage is
common when a person • Sudden, unusually severe headache and often
is active/ severe loss of consciousness
headache and nuchal
rigidity
• Pain and rigidity of the back of neck and
Cerebral Herniation of the brain Repeated vomiting spine due to meningeal irritation
stroke tissue à compressing Inability to stand or • Visuals disturbance (visual loss, diplopia,
medulla à increasing walk
pressure in the posterior Facial weakness
ptosis) occur if the aneurysm is adjacent to
fossa à cerebellar the oculomotor nerve. Tinnitus, dizziness,
bleeding and hemiparesis may also occur
Subarachnoid Weakeness of the artery Headache,
hemorrhage leading to leaking or confusion, vertigo, • Tinnitus, dizziness and hemiparesis
rupturing of the artery or fainting • If severe bleeding (raptured aneurysm)
occurs, cerebral damage followed rapidly
Leading cause: Trauma Loss of
consciousness may resulting to coma and death.
lead to lethargy
then coma
DIAGNOSTIC FINDINGS
• Cerebral angiography using the conventional
INTRACRANIAL ANEURYSM method or CT (CTA) confirms the diagnosis
Intracranial aneurysm (“cerebral aneurysm,"
of an intracranial aneurysm
"brain aneurysm") is a protruding bubble or sac on a
• These tests show the location and size of the
brain artery that balloons out over time.
lesion and provide information about the
affected arteries, veins, adjoining vessels,
Aneurysms have thin, weak walls and have a
and vascular branches
tendency to rupture causing hemorrhage into and
around vital brain structures.

Intracranial (cerebral) aneurysm is a dilation of MEDICAL AND PHARMACOLOGIC

the walls of a cerebral artery that develops as a result MANAGEMENT
of weakness in the arterial wall. These thin, weak • Analgesic agents may be prescribed for head
walls tend to rupture (raptured aneurysm) causing and neck pain. Fever should be treated with
hemorrhage into and around vital brain structures. acetaminophen (Tylenol), iced saline
The cause of aneurysms is unknown, although boluses, and devices such as cooling blanket.
research is ongoing. An aneurysm may be due to • After discharge, most patients will require
atherosclerosis, which results in a defect in the antihypertensive medications to decrease
vessel wall with subsequent weakness of the wall; a their risk of another intracerebral hemorrhage
congenital defect of the vessel wall; hypertensive • Administration of calcium channel blocker
vascular disease; head trauma; or advancing age (NIMODIPINE)

Site of aneurysm: Any artery within the brain can be SURGICAL MANAGEMENT
the site of a cerebral aneurysm. But it usually occur • The goal of surgery is to prevent bleeding in
at the bifurcations of the large arteries at the circle an unruptured aneurysm or further bleeding
of Willis. in an already ruptured aneurysm. This
objective is accomplished by isolating the
The cerebral arteries mostly affected by an aneurysm from its circulation or by
aneurysm: strengthening the arterial wall.
 • Aneurysm may be excluded from the cerebral impaired autoregulation increases the
circulation by means of a ligature or a clip chances of a cerebral infarction
across its neck
• If the aneurysm is very large or very wide at Implementing Aneurysm Precautions
its neck, a stent-like device made of a very • Placed patient on bed rest in a quiet, non-
fine mesh may be used to divert the blood stressful environment, because activity, pain,
flow away from the aneurysm. and anxiety are thought to elevate the blood
• Interventional neuroradiology for the pressure, which may increase the risk for
treatment of aneurysms– advance technology bleeding. Visitors may be restricted.
that commonly use now for the treatment of • The head of the bed is elevated 30 degrees to
aneurysm. promote venous drainage and decrease ICP
• Endovascular techniques may be used in • Any activity that suddenly increases the
selected patients to occlude the blood flow blood pressure or obstructs venous return is
from the artery that feeds the aneurysm with avoided (valsalva maneuver, straining,
coils, liquid embolic agents, or other forceful sneezing, pushing oneself up in bed
techniques to occlude the aneurysm itself. and acute flexion or rotation of the head and
neck (which compromises the jugular veins).
NURSING MANAGEMENT • Exhaling during repositioning should be
Assessment: advised
A complete neurologic assessment is • Stool softeners and mild laxatives are
performed initially and includes evaluation for the prescribed
following: Altered level of consciousness Sluggish • Dim lighting is helpful, because photophobia
pupillary reaction Motor and sensory dysfunction (visual intolerance of light) is common
Cranial nerve deficits (extraocular eye movements, • Relieving anxiety
facial droop, presence of ptosis) Speech difficulties • Monitoring and managing potential
and visual disturbance Headache and nuchal rigidity complications (vasospasm, seizures,
or other neurologic deficits re-bleeding aneurysm,
Hydrocephalus [blood in the
Nursing Diagnoses subarachnoid space or ventricles
• Risk for ineffective tissue perfusion impedes the circulation of CSF,
(cerebral) related to bleeding or vasospasm resulting in hydrocephalus]
• Anxiety related to illness and/or medically Evaluation
imposed restrictions (aneurysm precautions) Evaluate the effectiveness of the intervention. This
• Pain related to meningeal irritation may include:
1. Demonstrates stable neurologic status and
Planning and Goals vital signs and respiratory patterns within
Improved cerebral tissue perfusion, relief of anxiety, normal limits
and the absence of complications. 2. Exhibits reduced anxiety level
3. Free of complications
Nursing Interventions
Optimizing Cerebral Tissue Perfusion NEUROLOGIC TRAUMA
• The patient is closely monitored for Neurologic Trauma – trauma involving the central
neurologic deterioration resulting from nervous system that can be life threatening. If not life
bleeding, increasing ICP, or vasospasm threatening, brain and spinal cord injury (SCI) may
• A neurologic flow record is maintained. The result in major physical and psychological
blood pressure, pulse, level of consciousness dysfunction and can alter the patient’s life
(an indicator of cerebral perfusion), pupillary completely. Neurologic trauma involves trauma to the
responses, and motor function are checked scalp, skull and Brain & represent to the most cause of
hourly. death
• Respiratory status is monitored, because a
reduction in oxygen in areas of the brain with
Traumatic brain injury (TBI) or craniocerebral Signs and Symptoms:
trauma describes an injury that is the result of an • Period of unconsciousness lasting from a few
external force and is of sufficient magnitude to seconds to a few minutes
interfere with daily life and prompts the seeking of • Dizziness
treatment • Bizarre irrational behavior (frontal lobe
• Most common causes of TBIs are: affectation)
o Falls (35.2%) • Amnesia or Disorientations (Temporal lobe
o Motor vehicle crashes (17.3%) affectation)
o Being struck by objects (16.5%)
o Assaults (10%) Nursing Management:
• Children 0 to 4 years, adolescents 15 to 19 1. Provide information, explanations &
years, and adults 65 years and older are most encouragement to reduce post-concussion
likely to sustain a TBI. syndrome
• TBI rates are higher for males than for 2. Instruct SO to look for the following signs &
females notify physician such as difficulty in
awakening, difficulty in speaking, contusion,
CRANIO CEREBRAL TRAUMA (HEAD interactive discussion, severe headache,
INJURY) vomiting or weakness of one side of the body.
• Injuries to the head involves trauma to the 3. Advise client to resume activities slowly.
scalp, skull, and brain. This represents to the
most cause of death CONTUSION
Contusion - more severe cerebral injury. The brain
Possible causes: is bruised with possible surface hemorrhage.
• Falls • Petecchiation and Hemorrhage in cortex +/-
• Assaults edema and necrosis; Leading to focal signs
• Vehicular accident which can resolve or progress (Brainstem
• Sports injury hemorrhage more likely with twisting
impact.)
Major Risk Factors
• Traumatic brain injury Signs & Symptoms
• Damage to the brain from bleeding or • Client is unconscious
swelling that causes an increase in ICP • May exhibit faint pulse Shallow respiration
• Cool, pale skin
Craniocerebral Trauma Categories
1. Head Injuries, Closed- traumatic injuries to SECONDARY EFFECTS OF HEAD TRAUMA
the cranium where the integrity of the skull is • Trauma leads to pain, fear, and seizures
not compromised and no bone fragments or which result in increased cerebral
other objects penetrate the skull and dura metabolism. (Massive depolarization leads to
mater. It may produce traumatic brain increased ATP usage) The brain compensates
injuries, hemorrhage, or cranial nerve injury by vasodilating.
2. Head Injuries, Penetrating- features a
compromise of the skull and dura mater. MEDICAL AND/OR SURGICAL
• Maay result from gunshot wounds, stab MANAGEMENT:
wounds and other forms of trauma. 1. Mannitol Injection 20% is indicated for use
as an osmotic diuretic.
PRIMARY EFFECTS OF HEAD TRAUMA o Mannitol is essentially inert
CONCUSSION metabolically. When given
Concussion- transient loss of function without parenterally, it is freely filtered at the
obvious structural damage glomerulus which produces osmotic
diuresis as more than 90% of the
 mannitol injected escapes
reabsorption
2. Hyperventilation
PATHOPHYSIOLOGY OF TRAUMATIC
TWO FORMS OF TRAUMATIC BRAIN BRAIN INJURY
INJURY
1. Primary injury is defined as the
consequence of direct contact to the
head/brain during the instant of initial injury,
causing extracranial focal injuries (e.g.,
contusions, lacerations, external hematomas,
and skull fractures), as well as possible focal
brain injuries from sudden movement of the
brain within the cranial vault (e.g., subdural
hematomas (SDHs), concussion, diffuse
axonal injury [DAI])
2. Secondary injury evolves over the ensuing
hours and days after the initial injury and
results from inadequate delivery of nutrients
and oxygen to the cells. Contributors to this
process include intracranial pathologic
processes such as intracranial hemorrhage,
cerebral edema, intracranial hypertension,
hyperemia, seizures, and vasospasm SCALP INJURY
• Scalp trauma is generally classified as a minor
MONRO–KELLIE HYPOTHESIS injury.
• The cranial vault is a closed system, and if o Because its many blood vessels constrict
one of the three components increases in poorly, the scalp bleeds profusely when
volume, at least one of the other two must injured.
decrease in volume or the pressure will o A large avulsion (tearing away) of the
increase. scalp may be potentially life threatening
• Any bleeding or swelling within the skull and is a true emergency.
increases the volume of contents within the • Trauma may result in an abrasion (brush
skull and therefore causes increased wound), contusion, laceration, or hematoma
intracranial pressure (ICP). beneath the layers of tissue of the scalp
• If the pressure increases enough, it can cause (subgaleal hematoma).
displacement of the brain through or against • Scalp wounds are potential portals of entry for
the rigid structures of the skull. organisms that cause intracranial infections.
• This causes restriction of blood flow to the o The area should be irrigated before the
brain, decreasing oxygen delivery and waste laceration is sutured to remove foreign
removal. material and to reduce the risk for
• Cells within the brain become anoxic and infection
cannot metabolize properly, producing
ischemia, infarction, irreversible brain SKULL FRACTURES
damage, and eventually brain death Skull fracture is a break in the continuity of the skull
caused by forceful trauma. It may occur with or
without damage to the brain.
• Skull fractures are classified by type and
location.
• Types include linear, comminuted, and
depressed skull fractures, whereas location
 fractures include frontal, temporal, and basal
skull fractures.
o Simple (linear) fracture is a break in the MEDICAL MANAGEMENT
continuity of the bone. • Nondepressed skull fractures generally do
o Comminuted skull fracture refers to a not require surgical treatment; however,
splintered or multiple fracture line. close observation of the patient is essential.
o Depressed skull fractures occur when the o If the patient is discharged home,
bones of the skull are forcefully displaced specific instructions must be given to
downward, and can vary from a slight the family
depression to bones of the skull being • Depressed skull fractures usually require
splintered and embedded within brain surgery with elevation of the skull and
tissue. debridement, usually within 24 hours of
o Base of the skull fracture is referred to as injury.
a basal skull fracture
BRAIN INJURY
Types of fracture: Brain injury can cause significant brain damage
A. Open fracture - indicating a scalp laceration secondary to obstructed blood flow and decreased
or tear in the dura (e.g., from a bullet or an ice tissue perfusion.
pick) • The brain cannot store oxygen or glucose to
B. Closed fracture - Dura is intact. any significant degree.
• Because the cerebral cells need an
SIGNS AND SYMPTOMS uninterrupted blood supply to obtain these
• Persistent, localized pain usually suggests nutrients, irreversible brain damage and cell
that a fracture is present. death occur if the blood supply is interrupted
• Fractures of the cranial vault may or may not for even a few minutes.
produce swelling in the region of the fracture.
• Fractures of the base of the skull tend to Closed (blunt) traumatic brain injury occurs when
traverse the paranasal sinus of the frontal the head accelerates and then rapidly decelerates or
bone or the middle ear located in the temporal collides with another object (e.g., a wall, the
bone. Therefore, they frequently produce dashboard of a car) and brain tissue is damaged but
hemorrhage from the nose, pharynx, or ears, there is no opening through the skull and dura.
and blood may appear under the conjunctiva.
• An area of ecchymosis (bruising) may be Open (penetrating) traumatic brain injury -
seen over the mastoid (Battle sign). occurs when an object penetrates the skull, enters the
• Basal skull fractures are suspected when CSF brain, and damages the soft brain tissue in its path or
escapes from the ears (CSF otorrhea) and the when blunt trauma to the head is so severe that it
nose (CSF rhinorrhea). opens the scalp, skull, and dura to expose the brain
• Drainage of CSF is a serious problem,
because meningeal infection can occur if TYPES OF BRAIN INJURY
organisms gain access to the cranial contents A. Focal - focal injuries include contusions and
via the nose, ear, or sinus through a tear in the several types of hematomas
dura. B. Diffuse - concussions and diffuse axonal
injuries are the major diffuse injuries
DIAGNOSTIC FINDINGS
• A computed tomography (CT) scan can be FOCAL BRAIN INJURIES
used to diagnose a skull fracture. FOCAL CONTUSION
• If a fracture is found on CT scan, a magnetic • Occurs when the brain is bruised and damaged
resonance imaging (MRI) scan provides in a specific area because of severe
better resolution and clearer pictures of the acceleration–deceleration force or blunt
injured area trauma.
 • The impact of the brain against the skull leads SUBDURAL HEMATOMA
to a contusion. Subdural Hematoma
• Mostly occur in the anterior portions of the • Is a collection of blood between the dura and
frontal and temporal lobes, around the sylvian the brain; a space normally occupied by a thin
fissure, and at the orbital areas; cushion of fluid.
• Less commonly occur at the parietal and • The most common cause is trauma, but it can
occipital areas. also occur as a result of coagulopathies or
• Contusions can be characterized by loss of rupture of an aneurysm.
consciousness associated with stupor and • An SDH is more frequently venous in origin
confusion. and is caused by the rupture of small vessels
• The effects of injury, particularly hemorrhage that bridge the subdural space
and edema, peak after about 18 to 36 hours. • SDHs may be acute or chronic depending on
• These effects, which can cause secondary the size of the involved vessel and the amount
effects resulting in increased ICP and possible of bleeding on CT scan.
herniation syndromes, are most pronounced in
temporal lobe contusions. Acute Subdural Hematoma- associated with major
• Patients are most often managed medically head injury involving contusion or laceration.
with interventions directed toward prevention Clinical symptoms develop rapidly. Signs and
of additional insults. Deep contusions are more symptoms include changes in the level of
often associated with hemorrhage and consciousness (LOC), pupillary signs, and
destruction of the reticular activating fibers, hemiparesis. Craniotomy should be performed
altering arousal immediately to open the dura, allowing the subdural
clot to be evacuated. The mortality rate for patients
HEMATOMA with acute SDH is high because of associated brain
Hematoma- collections of blood in the brain that damage.
may be epidural (above the dura), subdural (below
the dura), or intracerebral (within the brain) Chronic Subdural Hematoma- develop from
• A rapidly developing hematoma, even if seemingly minor head injuries and is seen most
small, may be fatal, whereas a larger but frequently in older adults. Symptoms include severe
slowly developing one may allow headache, which tends to come and go; alternating
compensation for increases in ICP focal neurologic signs; personality changes; mental
deterioration; and focal seizures.

EPIDURAL HEMATOMA INTRACEREBRAL HEMORRHAGE AND

Epidural Hematoma HEMATOMA
• After a head injury, blood may collect in the Intracerebral Hemorrhage and Hematoma
epidural (extradural) space between the skull Intracerebral hemorrhage is bleeding into the
and the dura mater. parenchyma of the brain. It is commonly seen in head
• This can result from a skull fracture that injuries when force is exerted to the head over a small
causes a rupture or laceration of the middle area (e.g., missile injuries, bullet wounds, stab
meningeal artery, the artery that runs between injuries).
the dura and the skull inferior to a thin portion
of temporal bone.
• Hemorrhage from this artery causes rapid
pressure on the brain. Epidural hematomas
(EDHs) account for approximately 2.7% to
4% of traumatic head injuries
 Location of epidural, subdural, and maintained in alignment with the axis of the
intracerebral hematoma body.
• A cervical collar should be applied and
maintained until cervical spine x-rays have
been obtained and the absence of cervical SCI
documented.
• All therapy is directed toward preserving
brain homeostasis and preventing
secondary brain injury, which is injury to
the brain that occurs after the original
traumatic event
• Treatments to prevent secondary injury
include stabilization of cardiovascular
and respiratory function to maintain
adequate cerebral perfusion, control of
hemorrhage and hypovolemia, and
DIFFUSED HEAD TRAUMA maintenance of optimal blood gas values.
DIFFUSED CONCUSSION
• A concussion is a temporary loss of SURGICAL MANAGEMENT
neurologic function with no apparent • Surgery (craniotomy) is required for
structural damage to the brain. evacuation of blood clots. Debridement and
• Mechanism of injury is usually blunt trauma elevation of depressed fractures of the skull,
from an acceleration–deceleration force, a and suture of severe scalp lacerations may
direct blow, or a blast injury. also be performed
• If brain tissue in the frontal lobe is affected,
the patient may exhibit bizarre irrational SUPPORTIVE MEASURES
behaviour, whereas involvement of the • Ventilatory support, seizure prevention, fluid
temporal lobe can produce temporary and electrolyte maintenance, nutritional
amnesia or disorientation support, and management of pain and anxiety.
• Anticonvulsant if seizure occurs
DIFFUSE AXONAL INJURY (DAI) • Mannitol as an osmotic diuretic
• DAI results from widespread shearing and • Benzodiazepines are the most commonly used
rotational forces that produce damage sedative agents (if the patient is very agitated),
throughout the brain—to axons in the because it do not affect cerebral blood flow or
cerebral hemispheres, corpus callosum, and ICP.
brainstem o Lorazepam (Ativan) and midazolam
• It is more serious and is associated with a (Versed) are frequently used but have
poorer prognosis than a focal lesion. active metabolites that may cause
prolonged sedation, making it difficult
DIAGNOSTIC FINDINGS to conduct a neurologic assessment.
• Is made by clinical signs in conjunction with • Propofol (Diprivan), a sedative–hypnotic agent
a CT or MRI scan that is supplied in an intralipid emulsion for
intravenous (IV) use, is the sedative of choice.
MANAGEMENT o It is an ultra-short acting, rapid onset
MEDICAL MANAGEMENT drug with elimination half-life of less
• Assessment and diagnosis of the extent of than an hour. It has a major advantage
injury are accomplished by the initial of being titratable to its desired clinical
physical and neurologic examinations. effect but still provides the opportunity
• The patient is transported from the scene of for an accurate neurologic assessment
the injury on a board with the head and neck • A nasogastric tube may be inserted
 o Reduced gastric motility and reverse restlessness, or brain damage Risk for
peristalsis are associated with head imbalanced body temperature related to
injury, making regurgitation and damaged temperature-regulating
aspiration common in the first few mechanisms in the brain
hours. • Risk for impaired skin integrity related to bed
rest, hemiparesis, hemiplegia, immobility, or
NURSING MANAGEMENT restlessness
Assessment • Ineffective coping related to brain injury
• Elicit an information from the patient, from the • Disturbed sleep pattern related to brain injury
family, or from witnesses or emergency rescue and frequent neurologic checks
personnel. History should include the Planning and Goals
following questions: • Maintenance of a patent airway, adequate
• When did the injury occur? CPP, fluid and electrolyte balance, adequate
• What caused the injury? A high-velocity nutritional status, prevention of secondary
missile? An object striking the head? A fall? injury, maintenance of body temperature
• What was the direction and force of the blow? within normal limits, maintenance of skin
• Determine the patient’s LOC using the integrity, improvement of coping, and
Glasgow Coma Scale (GCS) and assessing the prevention of sleep deprivation
patient’s response to tactile stimuli (if
unconscious), pupillary response to light, Nursing Interventions
corneal and gag reflexes, and motor function • Maintaining optimal oxygenation to preserve
(Eye opening, verbal response, and motor cerebral function thru:
response to verbal command or painful stimuli) o elevation of the head of the bed about
30 degrees to decrease intracranial
Glasgow Coma Scale venous pressure
o Establishing effective suctioning
procedure
o Closely monitor arterial blood gas
values to assess the adequacy of
ventilation. The goal is to keep blood
gas values within normal limits to
ensure adequate cerebral blood flow.
o Monitor for pulmonary complications
such as acute respiratory distress
syndrome and pneumonia for patient
receiving mechanical ventilation
o Patient is at risk for ventilator-
Nursing Diagnosis associated pneumonia (VAP).
• Ineffective airway clearance and impaired Providing good oral hygiene can help
gas exchange related to brain injury prevent this complication
• Risk for ineffective cerebral tissue perfusion • Monitor fluid and electrolytes imbalance
related to increased ICP, decreased CPP, and • Promote adequate nutrition
possible seizures • Prevent injury
• Deficient fluid volume related to decreased • Maintain body temperature
LOC and hormonal dysfunction • Maintain skin integrity
• Imbalanced nutrition: less than body • Prevent sleep deprivation
requirements related to increased metabolic
demands, fluid restriction, and inadequate Evaluations
intake Expected patient outcomes may include:
• Risk for injury (self-directed and directed at • Attains or maintains effective airway
others) related to seizures, disorientation, clearance, ventilation, and brain oxygenation
 • Achieves satisfactory fluid and electrolyte
balance Medical and Surgical Management
• Attains adequate nutritional status • CT guided stereostatic needle aspiration
• Avoids injury • Pen G and Chloramphenicol, Corticosteroids,
• Maintains body temperature within normal and Anticonvulsants may be prescribed
limits
• Demonstrates intact skin integrity Signs and Symptoms
• Shows improvement in coping • Headaches usually worse in the morning
• Demonstrates usual sleep–wake cycle • Vomiting
• Family demonstrates adaptive family • Focal neurologic sign
processes o Focal neurologic signs “a hard,
• Demonstrates absence of complications localizing neurologic finding.”
• Loss of sensation in the distribution of a
SPINAL CORD INJURIES particular nerve
- Occurs predominantly in men as result of • Loss of vision in a well-defined portion of a
motor vehicular accidents, falls, gunshot visual field
wounds, and sports-related injuries injuries to
complete transection of the cord
- Most commonly occurs in cervical and lower MENINGITIS
thoracic-upper lumbar vertebrae. The brain and spinal cord are covered by three
connective tissue layers collectively called the
Signs and Symptoms (According to Level of meninges which form the blood-brain barrier
Injury): • Pia Mater (closest to the CNS)
• C1-C3: tetraplegia with total loss of • The arachnoid mater
muscular/ respiratory function • The dura matter (farthest from the CNS)
• C4-C5: tetraplegia with impairment, poor
pulmonary capacity, complete dependency The meninges contain cerebrospinal fluid (CSF)
for ADLs
• C6-C7: tetraplegia with some arm/hand Meningitis is an infection which causes
movement allowing some independence in inflammation of the membranes covering the brain.
ADLs If severe, it may become encephalitis, an
• C7-T1: tetraplegia with limited use of thumb, inflammation of the brain.
increasing independence • Non-bacterial meningitis is often referred to
• T2-L1: tetraplegia with intact arm function as “aseptic meningitis” e.g. viral meningitis
and varying function of intercostals and • Bacterial meningitis may be referred to as
abdominal muscles “purulent meningitis”
• L1-L2: mixed motor-sensory loss, bowel
bladder dysfunction

INFLAMMATORY DISEASES AFFECTING Causes and Risks

THE NEUROLOGIC SYSTEM The most common causes of meningitis are viral
BRAIN ABSCESS infections that usually resolve without treatment.
• Collection of infectious material within the 1. Inflammation- the cause could be viral or
tissue of the brain secondary to lymphoma, leukemia, or brain
• Fasciculations of one muscle group abscess
• Paresthesia or a reproducibly extra-brisk 2. Septic meningitis- refers to meningitis
knee jerk on one side are all “focal neurologic caused by bacteria, most commonly
signs.” a. Neisseria Meningiditis
• Change in mental status b. Haemophilus Influenzae
• Fever (not usually present in all cases) c. Streptococcus Pneumoniae
 • A spinal needle is inserted, usually
Risk Factors between the 3rd and 4th lumbar
1. Alcohol abuse vertebrae in the lower spine
2. Viral, upper respiratory infection because of • Permits the urgent distinction of
the increased amount of droplet production bacterial meningitis from viral
3. Otitis media and mastoiditis because it can meningitis and examination of the
cross the epithelium membranes and enter CSF allows precise diagnosis
the subarachnoid space
Nursing Management After the procedure:
Nursing Management: 1. Maintain client on NPO and flat on bed for 4-
1. To avoid further exposure, advise 6 hours to prevent post LP headache
individuals to: 2. Monitor neurologic status and vital signs and
a. Avoid sharing eating/drinking seize precaution
utensils 3. Maintain patient ET tube or tracheostomy for
b. Avoid sharing food, drinks, cigarettes, adequate ts. oxygenation
or musical mouth piece 4. Maintain thermoregulation
c. Cover mouth when sneezing/
coughing Pharmacotherapy
d. Washing hands frequently • Antimicrobial/Antibiotic (ampicillin,
2. To prevent additional cases piperacillin, ceftriaxone Na)
a. Advise contacts to seek medical • Vancomycin HCl alone or with Rifampicin
attention if symptoms of MM appear may be used if resistant stains of bacteria are
3. Other preventive measures to protect identified.
individuals • Dexamethasone for bacterial meningitis & in
a. Avoid smoking and smoky pneumococcal meningitis if given 15-
environment 20minutes before 1st dose of antibiotics q
b. Get plenty of sleep and exercise 6hrs for the next 4 days.
regularly • Phenytoin (Dilantin) for seizure
c. Eat a balanced diet and avoid
excessive alcohol consumption NEUROLOGIC DEGENERATIVE
d. Meningococcal vaccine is available DISORDERS
and should be offered to persons >2 MULTIPLE SCLEROSIS
years of age with • Chronic, progressive demyelinating disease
§ Travelers visiting meningitis of the CNS
belt • Small patches of demyelination of brain and
§ Persons who may be exposed spinal cord impair the transmission of nerve
to bacteria impulse

Signs and Symptoms of Meningeal Irritation Cause

• (+) Nuchal rigidity (stiff neck) is an early sign • Unknown but may be viral in origin or
• (+) Kernig’s sign- when the patient is lying secondary to autoimmune disease
with the thigh flexed on the abdomen, the leg
cannot be completely extended Goal of care: To delay the progression of disease
• (+) Brudzinski’s sign- when the patient’s
neck is flexed, flexion on the knees and hips Manifestations:
is produced • Onset: occurs in adult 20-40 y.o. (young
adult)
Diagnostic Tests for Meningism • Complains of urinary retention
1. Lumbar puncture- done to collect CSF to • Tinnitus (ringing of ears)
check for disease or injury • Slurred, hesitant speech as they have an
exacerbation of MS
• Difficulty with tremors and balance
 • Emotional labile (meaning the client may be PARKINSON’S DISEASE
laughing for one minute and suddenly cry) Parkinsonian Gait

Managements (No cure)

1. Treat the symptoms
• Adrenocorticotropic hormone (ACTC)
• Corticosteroids- decrease inflammation
or edema
• Stress management
• Immunosuppressant drugs
§ Azathioprine (Imuran)
§ Inferen Beta 1 B (betaseron)-
decrease exacerbation Festinating Gait is characterized by a flexed trunk
2. Encourage active life (Links to an external site.) with the legs flexed stiffly
3. Daily exercise- encourage swimming and at the knees and hips, arms do not swing.
station biking but discourage strenuous
exercises as this may lead to paresis or People with festinating gait take short steps, which
numbness eventually become faster to catch up with
4. Prevent injury him/herself, since his/her center of gravity (the part
• Avoid sressor that exacerbate the where the entire weight of the body is concentrated)
condition has been altered.

Manifestations based on the location of lesion: Pharmacotherapeutics

• Optic nerves: optic neuritis, blurring of • Carbidopa/Levodopa (Sinemet®)
vision, diplopia, scotoma (patchy blindness) Levodopa is a substance that is converted
• Cerebrum especially periventricular, frontal into dopamine by an enzyme in the brain.
and parietal lobes: cognitive and behavioral • It is then released by brain cells and activates
changes, dementia dopamine receptors allowing for normal
• Spinal cord especially cervical: weakness, function of the movement control centers of
spasticity, numbness, bladder, bowel, and the brain.
sexual dysfunctions • Levodopa is the “gold standard” by which
• Brainstem: vertigo, nystagmus, dysarthria all treatments for Parkinson’s is measured.
• Cerebellum and basal ganglia: ataxia, tremor, • Levodopa combined with carbidopa (or
emotional lability, euphoria Sinemet®) represented a significant
improvement in the treatment of Parkinson's
RING OR DONUT SCOTOMA disease.
A ring or donut-shaped scotoma is an area of • The addition of carbidopa prevents levodopa
reduced vision that forms a shape similar to a ring or from being converted into dopamine in the
donut. The patient can see fine in the center and off- bloodstream, allowing more of it to get to the
center a little bit but there is an area of reduced vision brain.
followed by another area of normal vision. • Stalevo® (carbidopa, levodopa and
entacapone) is a combination tablet for
Diagnostic Studies: patients who experience end-of-dose
• Lumbar puncture reveals elevated protein "wearing-off."
and gamma globulin o The tablet combines
• Electrophoresis of CSF reveals oligoclonal carbidopa/levodopa with entacapone.
banding o While carbidopa reduces the side
• MRI reveals presence of T3-T4 lesions of effects of levodopa, entacapone
greater than 3 mm in diameter of the brain extends the time levodopa is active in
the brain (up to 10 percent longer).
Cardinal Features: • Watch out for possible crisis
• Weakness
• Fatigability of muscles AMYOTROPHIC LATERAL SCLEROSIS
(LOU GEHRIG’S DISEASE)
Initial Signs : • Degenerative disease of the motor neurons in
• Ptosis the anterior horns of the spinal cord and
• Diplopia motor nuclei of the lower brain stem which
• Dysphagia results in muscular atrophy.
• Causes: Unknown
Investigative Studies • ALS affects 2- to 7 of every 100,000 persons,
• Anticholinesterase Testing with men affected about four times more
• Edrophonium (Tensilon) Test often than women; onset typically occurs
• 10mg Tensilon IV between ages 40 to 60 years old.
• Antibody Titer for AChR • In most cases death occurs within three to
• Elevated AChR antibody titer four years after the onset of symptoms.
• Repetitive Muscle Stimulation Inability to handle secretions and weakness
o Use of electrical shock of the respiratory muscles are the
• Single Fiber Electromyography predisposing causes of the usual TERMINAL
o 99% sensitive in confirming MG event, bronchopneumonia.
• Mediastinal MRI
o (+) enlargement of the thymus gland Clinical Manifestations:
• Lower Motor Neuron
Drug Therapy o Fasciculation
• Anticholinesterase Agent o Weakness
o Pyridostigmine (Mestinon) : Drug o Muscle Atrophy
of choice o Hyporeflexia
• Other Symptoms
Adverse Effect o Fatigue
• Muscarinic (Smooth Muscle) o Depression
• Diarrhea o Respiratory difficulty
• Bradycardia • Upper Motor Neuron
• Bronchospasm o Weakness
• Nicotinic (Skeletal Muscle) o Spasticity
• Muscle twitching , Muscle spasms o Impaired fine motor
• LMN & UMN (Brainstem)
Surgical Treatment : Thymectomy o Dysphagia
• Surgical removal of the thymus gland o Dysarthria
• 85% improvement o Dysphonia
Plasmapheresis
• Mechanical separation of pathologic Outcome Management : No known cure
antibody from blood
IV Immunoglobulin Investigative Studies
Adverse Effects • Electromyogram A of affected muscles will
• Headache reveal a reduction in the number of motor
• Fluid Overload units active on contraction, as well as
• Renal Failure (Rare) fasciculation and fibrillation.
• CPK
Nursing Care Focus o Elevated
• Medication administration
• Aspiration precaution Supportive Therapy
• Maintain adequate respiratory exchange • DRUGS and SPEECH THERAPY
• Maximize functional abilities 1. Muscle relaxant Speech Sensitizers
 2. Diazepam § Muscarinic (Smooth
3. Dantrolene Sodium Muscle)
• PHYSICAL THERAPY and § Diarrhea
OCCUPATIONAL THERAPY § Bradycardia
o Range of Motion § Bronchospasm
o Assistive devices
• Mechanical Ventilator and Gastrostomy Nicotinic (Skeletal Muscle)
Tube • Muscle twitching , Muscle spasms

MYASTHENIA GRAVIS Surgical Treatment : Thymectomy

• A neuromuscular disease affecting voluntary • Surgical removal of the thymus gland
muscles leading to muscular weakness and • 85% improvement
fatigue
• A defect in the transmission of impulses from Plasmapheresis
nerve to muscle cells results from loss or • Mechanical separation of pathologic
abnormal receptors (acetylcholine) from the antibody from blood
post-synaptic membrane of neuromuscular
junction IV Immunoglobulin
• Adverse Effects
Clinical Manifestations: o Headache
Clinical Features : o Fluid Overload
• Women : 20-30 yo o Renal Failure (Rare)
• Men : 50-60 yo
• W>M : 3:2 Nursing Care Focus
• Medication administration
Cardinal Features : • Aspiration precaution
• Weakness • Maintain adequate respiratory exchange
• Fatigability of muscles • Maximize functional abilities
• Watch out for possible crisis
Initial Signs :
• Ptosis HUNTINGTON’S DISEASE
• Diplopia
• Dysphagia

Investigative Studies
• Anticholinesterase Testing
• Edrophonium (Tensilon) Test
• 10mg Tensilon IV
• Antibody Titer for AChR
• Elevated AChR antibody titer
• Repetitive Muscle Stimulation
o Use of electrical shock • Is a progressive degenerative disease of the
• Single Fiber Electromyography basal ganglia and cerebral cortex beginning
o 99% sensitive in confirming MG in adult life and characterized by choreiform
• Mediastinal MRI movement and mental deterioration.
o (+) enlargement of the thymus gland • Caused by decreased of proteins or chemicals
Drug Therapy: such as GLUTAMIC ACID
• Anticholinesterase Agent DECARBOXYLASE and CHOLINE
o Pyridostigmine (Mestinon) - Drug ACETYLASE in the Basal Ganglia
of choice • Characterized by: Choreiform movement,
o Adverse Effects Lack of coordination, Dementia
Physical Manifestations • Medical Treatment
• Chorea o Immunotherapy
• Bradykinesia § IVIg (<2 weeks upon
• Dystonia diagnosis)
• Unsteady gait o Analgesia
• Slurring of speech § Pain episodes
• Dysphagia o Plasmapheresis
§ Mechanical separation of
GUILLAIN BARRE SYNDROME pathological antibodies
• is a disorder in which a person's immune o Mechanical Ventilation
system attacks the myelin sheaths that § Optimal O2 support
surrounds the axons of many peripheral Nursing Care Focus
nerves. • Assess respiratory function
• Administer oxygen as ordered
Signs and Symptoms • Be prepared for possible intubation
• Acute demyelination of both cranial and • Assess sensory & motor function
peripheral nerves (lower Motor Neuron • Monitor cardiac functions
Disease) • Hook patient to cardiac monitors
• Distribution of weakness progresses from • Take note of arrhythmias
lower to upper extremities (ascending), and
from distal to proximal
• Paresis in the legs ( initial stage ) DYSTONIA
• Tetraplegia with respiratory failure (late Definition: A group of movement disorders
stages) characterized by intense, irregular, sustained torsion
• Both female and male are at risk of the spasms of the musculature, with resultant marked
disease abnormalities of bodily posture

Causes : Viral Infection, campylobacter jejuni and CRANIAL NERVE DISORDERS

autoimmune TRIGEMINCAL NEURALGIA (TIC
DOULOUCREUX)
Major Symptoms: Loss of sensation, muscle • Affectation of the fifth cranial nerve
atrophy, weakness, diminished reflexes, pain and characterized by paroxysms of pain similar to
paresthesia of the extremities, rubbery like tingling an electric shock or burning sensation in the
sensations on the lower extremities and area innervated by the trigeminal nerve
AREFLEXIA ( neg (-) deep tendon reflexes) • Type of Pain : SHOOTING and STUBBING
Pain
Autonomic Features: Decreased or no sweating,
orthostatic hypotension, tachycardia and impotence, Medical Management
atrophic skin and nail changes, cardiac dysrhythmias Pharmacology
• Acute Onset • Anticonvulsant Drugs
o Appearance of definitive symptoms • Carbamazepine (Tegretol)– given with
o 1-3 weeks meals, in doses gradually increased until
• Plateau Period relief is achieved
o Several days to 2 weeks • Side effect: nausea, dizziness, drowsiness,
• Recovery Phase hepatic dysfunction
o Maximum recovery may takes 2 years • Phenytoin (Dilantin) reduce transmission of
impulses at certain nerve terminals to relieve
Diagnostic Tests : pain.
1. CSF Analysis _ elevated Protein • Gabapentin ( Neurontin) & Baclofen (
2. Nerve Conduction Velocity Test Lioresal)

Outcome Management Surgical procedures:

 • Nerve Block to decompress the trigeminal
nerve and relieves facial pain while
preserving the sensation.
• Percutaneous Radiofrequency Trigeminal
Gangliolysis - provides permanent pain relief
• Injection of alcohol or phenol into the
gasserian ganglion & peripheral branches to
relieve pain for several months.

BELL’S PALSY (FACIAL PARALYSIS)

• Weakness and paralysis of the facial muscles

on one side due to peripheral involvement of
the seventh cranial nerve
• Characterized by increased lacrimation,
painful sensations in the face, behind the ear
and in the eye, and distortion of face.

Medical and/or Surgical Management

• Corticosteroids to reduce edema &
inflammation & relieve pain
• Analgesics may be given to minimize facial
pain
 FAR EASTERN UNIVERSITY
Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Module 4 Care of Clients with Ear and Eye Problems
Review of Anatomy and Physiology of the Eyes and Ears

OUTLINE: • The eyelashes on the edge of the lids prevent

1. Eyes foreign particles from entering the eye.
a. External Structures of the Eye • The meibomian glands line the upper and
b. Three Layers of the Eyes lower lid, producing sebum, an oily secretion
c. Functions of the Major Parts that mixes with the tears to keep the eyelids
d. How sight works from sticking together.
e. Common Eye Disorders • The eyelids form a canthus (an angle of skin)
2. Ears at the inside and outside corners of the eye.
a. External ear
b. Middle ear Conjunctiva- he lining on the underside of each
c. Inner ear eyelid and the mucous membrane over the eyeball,
providing a protective covering for the exposed
REVIEW OF ANATOMY AND PHYSIOLOGY surface.
OF THE EYES AND EARS
EYES Lacrimal apparatus- includes the structures that
The eye is composed of several structures that work produce, store, and remove tears that cleanse and
together to facilitate sight. Vision is possible through lubricate the eye. The lacrimal glands secrete the
the coordination of nerves that control movement of tears that wash across the conjunctiva during
the eyeball, the amount of light admitted by the pupil, blinking.
the focusing of light on the retina by the lens, and the • Lacrimal canaliculi are the two ducts at the
transmission of the impulses to the brain by the optic inner corner of the eye that collect tears.
nerve. • Lacrimal sac dilates and pulls in the tear
fluid.
EXTERNAL STRUCTURES OF THE EYE • Nasolacrimal duct drains the tears into the
Orbit- a cavity in front of the skull that contains the nose.
eyeball. It is formed by several bones and lined with
a fatty tissue that cushions the eyeball. It has several Eyeball- is globe-shaped and divided into two
openings or foramina for blood vessels cavities. At the front is a cavity filled with a watery
and nerves, including the optic foramen for the optic fluid called the aqueous humor. At the back is a
nerve and ophthalmic artery. cavity filled with a jelly-like material called the
vitreous humor, which maintains the shape of the
Eye muscles- Six muscles control eye movement; eyeball.
four are rectus muscles that allow a person to see up,
down, right, and left; the other two are oblique Outer layer- has two parts:
muscles that allow the eyes to turn to see upper left • Sclera is the white of the eye.
and upper right, and lower left and lower right. The
• Cornea is the transparent outer surface. It is
muscles also maintain the shape of the eyeball.
curved, which bends light rays and helps to
focus them on the surface of the retina.
Eyelids- The superior and inferior palpebrae
are the upper and lower eyelids. They protect the
Middle layer- the middle layer of the eyeball, just
eyeball from intense light, foreign particles and
behind the transparent cornea, contains the colored
impact. Their blinking motion keeps the eyeball’s
iris. It has a hole in the center called the pupil, which
surface lubricated and free from dust and debris.
contracts and dilates to regulate the amount of light
admitted. The ciliary body controls the convexity of Choroid Layer - middle layer of the eye containing
the lens and secretes aqueous humor. The choroid is may blood vessels
a pigmented membrane that prevents internal Ciliary Body - the ciliary body is a circular band of
reflection of light. muscle that is connected and sits immediately behind
the iris- produces aqueous humor, changes shape of
Inner layer- The innermost layer of the eye is the lens for focusing
retina, which is full of photoreceptive cells called
rods and cones. Iris - the pigmented front portion of the choroid layer
• The rods are sensitive to dim light and are and contains the blood vessels - it determines the eye
used for night vision. color and it controls the amount of light that enters
• The cones are sensitive to bright light and the eye by changing the size of the pupil (an albino
used for color vision. only has the blood vessels – not pigment so it appears
• Nerve fibers from the retina all converge to red or pink because of the blood vessels)
form the optic nerve at a spot on the inner
layer known as the optic disk. The optic nerve Lens - a crystalline structure located just behind the
goes directly to the vision center of the brain. iris - it focuses light onto the retina
There are no rods or cones in the area of the
optic disk, so it is insensitive to light and a Pupil - the opening in the center of the iris- it
blind spot is created. changes size as the amount of light changes (the more
light, the smaller the hole)
Lens- a colorless crystalline body that contracts and
relaxes due to the action of the ciliary muscle. These Vitreous - a thick, transparent liquid that fills the
changes in the shape of the lens is called center of the eye - it is mostly water and gives the eye
‘accommodation’, and occurs for near and distant its form and shape (also called the vitreous humor)

THREE LAYERS OF THE EYES Retina - sensory tissue that lines the back of the eye.
1. Outer layer consists of sclera and cornea It contains millions of photoreceptors (rods for
2. Middle layer consists of choroid, ciliary black & white and cones for color ) that convert
body and iris light rays into electrical impulses that are relayed to
3. Inner layer consists of retina the brain via the optic nerve

FUNCTIONS OF THE MAJOR PARTS OF Optic nerve - the nerve that transmits electrical
THE EYE impulses from the retina to the brain
Sclera or Scleroid Layer (white of eye)- a tough
protective layer of connective tissue that helps HOW SIGHT WORKS
maintain the shape of the eye and provides an As you view an object, the light rays strike the eye
attachment for the muscles that move the eye and pass through the cornea, pupil, aqueous humor,
lens, and vitreous humor, and reach the retina. The
Cornea - the clear, dome-shaped part of the sclera image stimulates the rods and cones and an upside-
covering the front of the eye through which light down image is transferred to the brain. The brain
enters the eye turns the images right-side up

Anterior Chamber – a small chamber between the COMMON EYE DEFECTS

cornea and the pupil • Myopia or nearsightedness where the
eyeball is too long or the cornea is too steep
Aqueous Humor - the clear fluid that fills that • Hyperopia or far sightedness where the
anterior chamber of the eye and helps to maintain the eyeball is short or lens cannot become round
shape of the cornea providing most of the nutrients enough
for the lens and the cornea and involved in waste • Cataracts where the lens becomes fogged
management in the front of the eye
 • Presbyopia where the muscles controlling There are holes in the cochlea, round and oval
the bulging of the lens become weak as we windows, allowing sound to enter it from the middle
age ear.
• Nyctalopia or night blindness where vision
is impaired in dim light and in the dark due Inside one of the cochlea chambers is the organ of
to pigment rhodopsin in the rods not Corti. It is filled with nerve endings that connect to
functioning properly the auditory nerve, transmitting sounds from the
inner ear to the brain.
EARS
The ear is designed for hearing and equilibrium. It The vestibule and semicircular canals are bony
receives sound vibrations, is sensitive to the force of structures lined with membranes and containing a
gravity, and reacts to the movement of the head. fluid called perilymph which provides a sense of
equilibrium. Changes in the position of the head
EXTERNAL EAR cause this fluid to move against sensory receptors.
The external ear consists of the cartilaginous pinna Dizziness or motion sickness may be associated with
projection that collects and channels sound, the ear rapid movements.
canal or auditory canal which opens the eardrum
or tympanic membrane that vibrates as the sound
hits it.

Glands line the auditory canal and secrete cerumen

or earwax. This lubricates and protects the ears.

MIDDLE EAR
The middle ear contains three small bones or
ossicles: malleus, incus, and stapes.

Malleus or hammer connects to the tympanic

membrane on one side and the incus or anvil on the
other. The incus then connected to the stapes or
stirrup. As the sound vibrations are transmitted
mechanically through these bones, it is amplified up
to 22 times.

The middle ear is also responsible for equalizing

external and internal air pressure on the tympanic
membrane. This occurs when air comes in from the
inside through the throat and eustachian tube.

Muscles near the inner ear attach to the stapes and

malleus, exerting some control over damaging loud
sounds.

INNER EAR
The inner ear contains structures referred to as
labyrinths, because they are complicated, bony
shapes.

One of these structures is called the cochlea. It is

divided into 3 channels that run its entire coiled
length. These channels are filled with auditory fluids
 FAR EASTERN UNIVERSITY
Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Ears and Eyes
Care of Clients with Visual Problems

OUTLINE • Administer mydriatics/ cyciopegics as

1. Care of Clients with Visual and Problems prescribed
2. Common Disorders of the Eye o Isopto Atropine, Oculropine,
a. Eyelid Disorders Atropair, Atropisol (Atropine Sulfate)
b. Extraocular Muscle Disorders o Cyclomydril (Cyclopentolate and
c. Uveal Tract Disorders Phenylephrine)
d. Retinal Disorders o Cyclogyl (Cyclopentolate HCl)
e. Glaucoma o Scopolamine
f. Cataract o Mydriacyl (Tropicamide)
g. Tumors of the Eye and Related • Mydriatics and cyclopegies dilate the pupils
Structures (mydriasis) and relax the ciliary muscles
(cyclopegia)
PHYSICAL ASSESSMENT OF THE EYES o These mediation are contraindicated
• Snellen chart o E chart for testing visional in glaucoma because of the risk of
acuity; at 20 feet increase in intraocular pressure
• Cardinal fields- test for extraocular
movement POST-OPERATIVE CARE OF THE CLIENT
• Cover-uncover test- test for stabismus IN EYE SURGERY
General Goals of Post-operative Care:
CARE OF CLIENTS WITH VISUAL • To prevent or relive the following:
PROBLEMS o Increased intraocular pressure
VISION PROTECTION AND GENERAL EYE o Stress on the suture side
CARE o Hemorrahe into the anterior chamber
• Regular ocular and physical examinations (hyphema)
• Avoid dangerous items (toys, guns, arrows, o Infection
fireworks rocks, sticks, etc.) o Pain
• Early identification and treatment of
strabismus in children Management:
• Routine eye assessment programs in schools 1. Position the client supine or turned to the
• Early treatment when eye symptoms occur unaffected side to prevent pressure on the
• Avoid rubbing of the eyes operated eye and to prevent possible
contamination of the dressings with vomitus
• Adequate lighting
2. A burning sensation about one hour after the
• Periodical eye rest during prolonged close
surgery usually means that the anesthetics is
eye work
wearing off. This is normal
3. The eye is protected with eye patch and eye
PREOPERATIVE CARE OF THE CLIENT
shield for 5-7 days
FOR EYE SURGERY
a. Use eye shield during the night for 4
• Orient the client to the staff and physical weeks
environment if both eyes will be covered 4. The client should be instructed to avoid the
after surgery
following to prevent increase in intraocular
• If the client is a child, practice covering the pressure
eyes a. Rubbing the eyes
 b. Lifting the head or hips o Hypotropia- downward (“sunset
c. Sudden, jerky head movement eyes”)
d. Sneezing, coughing (follow through
with open mouth if these cannot be Collaborative Management
prevented) • Corrective eyeglasses
e. Nausea and vomiting (keep eyelids • Surgery
open if vomiting occurs) o Advancement, resection, tucking
f. Straining at stool o Tenotomy, recession
g. Bending, stooping NoteL Cover/ patch the “good eye” to train the “bad
h. Heavy lifting (more than 5 lbs) eye.”
i. Reading (for few days)
j. Watching fastmoving objects) DISORDERS OF THE CONJUNCTIVA,
5. The feeling of “something in the eye” 4 to SCLERA, AND CORNEA
days postop is usually because of the sutures. Conjunctivitis- inflammation which results from
This is normal. bacterial or viral infections
6. Sensation of pressure within the eye and - Redness. Swelling, lacrimation, pain, itching,
sharp pain in the eye indicate bleeding. These discharge from the eye
should be reported to the surgeon - E.g. bacterial, gonococcal conjunctivitis
immediately.
7. Administer miotics as prescribed. These Trachoma- a chronic infectious disease of the
medications constrict the pupils. conjunctiva and comes caused by Chamydia
a. Carbotic (Carbachol) trachomatis
b. Humorsol (Demecarium Bromide) - Spread by direct contact and very contagious,
c. Floropryl (Isoflurophate) causes blindness
d. Isopto Carpine (Pilocarpine HCl) - Treatment: sulfonamides, tetracyclines,
erythromycin
COMMON EYE DISORDERS
EYELID DISORDERS Scleritis/Iritis- inflammation of the sclera
Blepharitis- inflammation of eyelid margins - Very red eye, painful to move
- Irritation, burning, itching, ulceration,
eyelashes fall out Corneal Inflammation (Keratitis) and Corneal
Ulceration
Chalazion- internal stye; “kuliti” • Assessment: pain, photophobia, lacrimation,
- Inflammation of Meibomian gland blepharospasm, decreased vision
- Painless, slow growing, hard, nontender • Treatment:
round mass on eyelid o Trifluridine (Viroptic), Idoxurindine
(IDU), Adenine Arabinosode (Vira-
Hordeolum- external stye A)
- Pustular infection of eyelash follicle or o Mechanical or chemical debridement
sebaceous gland on an eyelid margin
- Painful, red swelling on eyelid margin Conceal Ulcerations- medical emergency
- Commonly caused by staphylococcus - May result to corneal perforation, scarring, or
intraocular infection, permanent impairment
EXTRAOCULAR MUSCLE DISORDERS of vision
Strabismus (squint, tropia, heterotropia) - Causes: trauma, exposure, allergy, vitamin
- Conditions in which cannot consistently deficiency, lowered resistance, bacterial,
focus two eyes simultaneously on the same viral, or fungal infections
object
- Eye deviations Corneal Opacity- lack of corneal transparency due
o Esotropia- inward/convergent to inflammation, ulceration
o Exotropia- outward/divergent
o Hypertropia- upward (“sunrise eyes)”
 • Conceal Transplantation (Keratoplasty)- to SYMPATHETIC OPTHALMIA
repair corneal opacity, perforation of corneal (SYMPATHETIC UVEITIS)
ulcer • A rare, severe, bilateral, granulomatous
o Donor eyes for corneal uveitis of unknown cause
transplantations come from cadavers • Occurs anytime from 10 days to several years
o Ideally, a donated eye is transplanted following a penetrating injury near the ciliary
immediately or is removed from the body or following a retained foreign object
body within 24 hours of death. • Leads to bilateral blindness
Cornea may still be viable within 12
hours after death if the body has been Assessment
refrigerated, may be transplanted up • Inflammation of the injured or previously
to 48 hours after death if its kept at a operated eye (exciting eye), followed by the
sterile container, on a piece of gauze other eye (sympathizing eye)
soaked in NSS at 4°C • Photophobia
• Blurred vision
UVEAL TRACT DISODERS
Uveal Tract is the middle vascular layer of the eye, Collaborative Management
contributing to the retina's blood supply- lt is • Enucleation- done if the with perforation of
composed of iris, ciliary body, and choroid sclera and ciliary body, vitreous humor loss,
retinal damage
UVEITIS • Steroids
• Iritis- inflammation of iris • Local atropine
• Iridocyclitis- inflammation of the iris and
ciliary body RETINAL DISORDERS
• Choroiditis - inflammation of the choroid RETINITIS
• Choroiretinitis - inflammation of choroid • inflammation of the retina
and retina • often associated with disease of the choroid
• Caused by bacteria, fungi, toxoplasmosis,
Causes: local or systemic disease, injury, cytomegalovirus
unidentified factors • Assessed through ophthalmoscopy
o Reduced visual acuity changes in the
Assessment visual field
• Pain in the eyeball radiating to the forehead o Alterations in the shapes of objects
and temple. o Discomfort in the eyes
• Blurred vision
• Redness of eyes without purulent discharge Collaborative Management
• Small pupil • Rest the eyes
• Lacrimation • Protect the eyes from sunlight
• Atropine sulfate
Collaborative Management
• Mydiatics (Atropine Sulfate 1% or 25%,
RETINAL DETACHMENT
Scopolamine) • Separation of the two primitive layers of the
o To dilate pupils
retina (melanin epithelial pigment and the
o To prevent adhesion between anterior rods and cones layer). Or it may be separation
capsule of the lens and the iris of the entire retina from the choroid due to the
o To relieve pain and photophobia presence of a tumor
o To reduce congestion
o To rest the iris and the ciliary body
Causes:
• Steroids (local/systemic)
• Myopic degeneration, trauma, hemorrhage,
• Dark glasses (to relieve exudates in front or behind the retina, aphakia
• Analgesics (Aspirin, Acetaminophen)
 (absence of lens), sudden and severe physical caused by an imbalance in production and
exertion among debilitated clients excretion of aqueous humor. It is the result of
an abnormal displacement of iris against the
Clinical Manifestations angle of the anterior chamber
• Floating spots or opacities before the eyes.
These are blood retinal cells that cast Assessment For Acute Glaucoma
shadows on the retina • Rapid onset of severe pain in eye(s)
• Flashes of light. The light that enters the eye • Blurred vision
is not absorbed by the detached melanin • Headache
epithelial pigment. • Rainbows or halos around lights
• Progressive constriction of vision in one area. • Nausea and vomiting
There is sensation that a curtain has been • Inflamed eye(s)
drawn before the eyes or as if one is looking • Fixed, dilated
over a fence • Visual impairment
• Ophthalmoscopy shows cloudy vitreous and
portion of retina appears like a hanging gray Collaborative Management For Acute Glaucoma
cloud. • Maintain bed rest in quiet, darkened elevate
head 30°
Collaborative Management • Monitor vital signs.
• Promote bed rest and cover the eyes to • Administer miotic eyedrops as ordered
prevent further detachment • Administer acetazolamide, glycerol orally as
• Position the head so that retinal hole is in the ordered.
lowest part of the eye (dependent position) • Acetazolamide is carbonic anhydrase
• Early surgery is required (e.g. scleral inhibitor. lt reduces aqueous humor Thereby,
buckling) decreasing intraocular pressure.
• Preop care (refer to the Care of Client for Eye • Glycerol is an osmotic drug which act to
Surgery) reduce intraocular
• Postop care: • Provide emotional support.
o Position: the area affected should be • Assess patient's ability to see.
in upper part of the eye (superior • Assist according to degree of visual
position) impairment.
o Activity and ambulation will be • Prepare for eye examinations as ordered
prescribed by the surgeon tonometry is 25 mmHg and above in
o Sedentary activities are resumed after glaucoma).
three weeks • Avoid Atropine preparations and other
o Activities or occupations requiring mydriatics. These dilate the pupils, and the
heavy physical exertion may be iris is brought closer to the angle of outflow
permitted after 6 weeks of aqueous humor. This causes further
obstruction in the excretion of aqueous
GLAUCOMA humor. In glaucoma, avoid ABC:
• Is an eye disorder characterized by increase o A tropine
in intraocular pressure o B enadryl
o C ogentin
Aqueous humor- crystal clear fluid, fills the anterior • Administer antiemetics as ordered for nausea
and posterior chambers of the eye. It is a refraction • Provide diet as tolerated.
medium, provides nutrition to the lens and cornea, • Prepare for surgery if ordered
helps maintain IOP
CHRONIC GLAUCOMA (SIMPLE, WIDE
ACUTE GLAUCOMA (NARROW ANGLE OR ANGLE OR OPEN ANGLE GLAUCOMA)
CLOSE ANGLE GLAUCOMA) • Eye disease characterized by impaired vision
• Eye disease characterized by suddenly due to intraocular tension caused by an actual
impaired vision due to intraocular tension obstruction in the excretion of aqueous
 humor. It develops slowly at first, symptoms • The patient is advised to avoid fatigue or
may be absent stress and to avoid drinking large quantities
• It may be due to hereditary thickening of the of fluids
trabecular meshwork or degenerative • Surgery: sclerotomy, iridectomy,
narrowing of the canal of Schlemm iridendeisis, trabeculectomy, and trephine
• Vision loss in glaucoma is irreversible due to operations
compression and damage of the retina and/or
optic nerve NURSING DIAGNOSES FOR THE PATIENT
• The blockage of the circulation of the WITH GLAUCOMA
aqueous humor may be secondary to: • Risk for injury related to visual acuity deficits
o Infection e.g. uveitis (acute • Self-care deficits related to visual acuity
glaucoma) deficits
o Injury (acute glaucoma) • Acute pain related to pathophysiologic
o Hereditary predisposition to the process and surgical correction
thickening of the trabecular • Noncompliance related to inconvenience and
meshwork (found at the angle of the side effects of glaucoma medications
anterior chamber of the eye where the
peripheral iris and the cornea meet DRUG THERAPY IN ACUTE AND CHRONIC
(chronic glaucoma) GLAUCOMA
o Narrowing of the canal of Schlemm
Beta-adrenergic blockers
(chronic glaucoma) • These drugs decrease aqueous humor
production
CHRONIC / SIMPLE GLAUCOMA o Betaxolol (Betoptic)
Assessment o Carteolol (Ocupress)
• Character sign: before central vision is
o Levobunolol (Betagan)
affected, the peripheral visual fields are o Metipranolol (Optipranolol)
impaired so that objects to the side are o Timolol Maleate (Timoptic, lstalol)
ignored (tunnel vision) o Alpha-adrenergic Agonist
• Insidious onset generally no discomfort
• Patients may bump into other person in the
CATARACTS
street or fail to see passing vehicles, yet not Cataract is a clouding, or opacity of the lens that
realize that the fault lies on their own vision leads to blurring of vision and eventual loss of sight.
• Persistent dull eye pain in the morning
The opacity of the lens is caused by chemical
• Frequent changes of glasses, difficulty in
changes in the protein of the lens because of slow
adjusting to darkness degenerative changes of age, injury, poison or
• Failure to detect changes in color accurately
intraocular
Collaborative Management Cataracts occur so often in the aged. At 80 years of
• Objective: To reduce intraocular pressure age, about 85% of all people have some clouding of
and keep it at a safe level the lens.
• Miotics. Used to constrict the pupil and to
draw the smooth muscle of the iris away from Classification of Cataracts
the canal of Schlemm to permit aqueous • Senile. Those associated with aging.
humor to drain out at this point • Traumatic. Those associated with injury.
• Drug Alert: Miotics • Congenital. Those that occur at birth
o Warn patients about decreased visual • Secondary. Those that occur following other
acuity especially in the daylight eye or systemic
• Acetazolamide (Diamox). A drug that tends
to reduce the formation of aqueous humor; is
used successfully for some types of chronic
glaucoma.
Collaborative Management For Cataracts • Use of contact lens improves visual
• Surgery is the only satisfactory treatment for correction and better in cosmetic appearance
cataracts. It is advised when the cataract
interfere with a person’s mobility Intraocular lens implant. An alternative to cataract
o Intracapsular technique. Removal glasses and contact lenses. The lens, which is made
of cataract within its capsule (ICCE) of polylethyl methacrylate, is implanted at the time
o Extracapsular technique. An of cataract extraction. It may be held in position
opening is made in the capsule and either by suture to the iris or by implanting it into the
the lens is lifted without disturbing capsular sac (the main advantage of the implanted
the membrane. A person with aphakia lens is better binocular vision).
is very farsighted (hyperopic)
(ECCE) TUMORS OF THE EYE AND RELATED
o Cryoextraction. The cataract is lifted STRUCTURES
from the eye by a small probe that has • Benign or malignant tumors
been cooled to a temperature below • Displace the eyeball and interfere with
zero and adheres to the wet surface of vision.
the cataract • Retinoblastomas (children), malignant
o Indectomy. Done preceding cataract melanomas (adult):
extraction to create an opening for the o Are the most common primary
flow of the aqueous humor which intraocular
may become blocked post op when
the vitreous humor moves forward. REFRACTION ERRORS
This is to prevent secondary • Emmetropia. Normal refractive state
glaucoma. • Ammetropia. Abnormal refractive state.
o Phacoemulsion. A method of "Sight not in proper measure”
cataract removal which breaks up the • Hyperopia - Farsightedness
lens and flushes it out in tiny pieces o Parallel rays of light focus behind the
Preop care: refer to General Care for Eye Surgery retina.
o Corrected with convex lens.
Postop Care • Myopia - Nearsightedness.
• The eye is covered with a dressing (eyepad) o Parallel rays of light focus in front of
and eye shield to protect it from injury the retina.
• The patient is usually allowed out of bed the o Corrected with concave lens.
day following surgery o Radial keratotomy (RK Surgery).
• Daily change of dressing is done. After 7 to • Presbyopia- “old sight”
10 days at night o Lessening of the effective powers of
• Administer eye drops as ordered accommodation, occurs because of
hardening of the lens due to aging
Note: process
• Temporary glasses may be prescribed 1 to 4 o Blurring of near objects or visual
weeks after the surgery. Usually within 6 to fatigue when doing “close eye work”
12 weeks healing has been sufficient of o Convex reading glasses are
permanent glasses or contact lenses recommended
• Astigmatism- "Distorted vision"
Remember: o Caused by variation in refractive
• Cataract glasses (aphakik glasses) magnify so power along different meridians of
that everything appears about one-fourth the eye.
closer than it is. Patients need to know that it o Optical distortion is most often
will take time to learn to judge distance, to caused by irregular corneal curvature,
climb stairs, and do other simple things which prevents clear focus of light
from any point.
 • Aphakia - Is the absence of lens. It may be • Laser Thermal Keratoplasty and conductive
absent congenitally or it may be removed keratoplasty are indicated for patients with
during cataract hyperopia and presbyopia
• These procedure use laser or high radio
NON SURGICAL CORRECTIONS frequency and heat is applied to the
Corrective Glasses peripheral area of the cornea to tighten it like
• Myopia requires concave lens a belt and make the central cornea steeper
• Hyperopia, aphakia, presbyopia
require convex lens DIABETIC RETINOPATHY
• Glasses for presbyopia are often called • Leading cause of new blindness between ages
"reading glasses” because they are usually of 20-74
worn for close work • 84% of diabetics will develop some form
• Presbyopia maybe corrected with the "no- o Depends on the length of time one has
line' bifocal which is actually a multifocal diabetes
lens that allows the patient to see clearly at • Vascular disorder that affects the retina
any distance. o Capillaries become sclerotic
Contact Lenses Management
• These are made of plastic and silicone
• Yearly ophthalmologic exams
substances which are very permeable to
• Laser photocoagulation
oxygen and have high water content which
• Focus is educational
allows greater wearing time with greater
o Vision changes- blurred
• The patient should know the signs and
o Black spots (Floaters)
symptoms of contact lens problems that must
o Flashing lights
be managed by the eye care professional
o Sudden loss of vision
which are as follows (DANGER SIGNS -
TRAUMA TO THE EYE AND RELATED
RSVP):
STRUCTURES
o Redness
PENETRATING EYE INJURIES
o Sensitiveness
• Requires surgery (repair/enucleation).
o Vision Problems
• Bed rest with bathroom privileges for 1 to 2
o Pain
days. Do not strain.
• Observe for sympathetic ophthalmia.
Corneal molding- also called orthokeratology
• It is the use of specially designed, rigid, gas INTRAOCULAR FOREIGN BODIES
permeable contact lenses to alter the shape of
• Wash hands thoroughly before touching the
the cornea eye
• It reduces or corrects myopia and moderate • Immediate copious flushing of the eye with
degrees of astigmatism water when acid, alkali or other irritating
substance has been introduced.
SURGICAL THERAPY • If foreign body is lodged into the comes, do
Laser not attempt to remove, see a physician.
• Laser-assisted-in-situ keratomileusis • Avoid pressure on the eye, do not touch, do
(LASIK) maybe considered for patients with not rub the eye.
low to moderately high amounts of myopia, • Cover with dressing or plastic or metal eye
hyperopia, and astigmatism shield for protection, to limit eye movement
and prevent further
Refractive intraocular lens implant- it is usually • Avoid activities that increase IOP.
done following cataract removal • Use sterile technique, when treating the eyes.
• Consult ophthalmologist
Thermal Procedure
 SYMPATHETIC OPHTHALMIA
Occurs from 10 days to several years following
penetrating injury near the ciliary body or retention
of foreign body in the eye. This may lead to bilateral
blindness. This requires enucleation, steroids, topical
atropine.

EYE SURGERIES
• Enucleation. Removal of the eyeball.
• Evisceration. Removal of the entire eyeball
contents and comes, except the sclera.
• Exanteration. Removal of the eyelid,
eyeball and orbital contents.

LEGAL BLINDNESS
• Central visual acuity for distance of 20/200 or
worse in the better eye (with correction)
• Visual field no greater than 20 degrees in its
widest diameter or in the better

REHABILITATION OF A BLIND PERSON

• Refer blind persons to available facilities.
• Orient to the environment. Describe the
surroundings and things.
• Promote independence through ADL
(Activities of Daily living).
• May have a guide or use cane for
• When approaching talk before touching.
• When assisting in ambulation, have the
patient hold your forearm so that you are a
step ahead of him.
• Talk to the patient frequently, so he I she
doesn't feel neglected.
• Be relaxed and unhurried when performing
nursing procedures.
• Explain what is being done and what is to be
done next.
• Do not change location of objects in the room
or in the environment without describing the
• Promote safety in the environment.
• Do not rush up and offer help to a blind
person unless it is clear that the person wants
help.
• If significant others ask advise about gifts for
a blind person, suggest gifts that appeal to
senses other than vision (i.e. stuff toys,
perfume, music devices)
 FAR EASTERN UNIVERSITY
Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Ears and Eyes
Care of Clients with Auditory Problems

OUTLINE o Normal: tone is heard in center of

1. Diagnostic Tests for Auditory Acuity head or equally in both ears.
2. Symptoms of Ear Disorders o Conductive hearing loss- tone is
3. Classifications of Hearing Loss heard in poorer ear, e.g. otosclerosis
4. Assessment of Client with Hearing Loss o Sensorineural hearing loss: tone is
5. Guidelines for Communicating with the heard in better
Client with Hearing impairment • The test is useful in cases of unilateral
6. Communication with Hearing Impaired • It is more accurate in diagnosing
Patient sensorineural hearing loss like in Meniere's
7. Diseases of the Outer Ear disease.
8. Diseases of the Inner Ear
9. Different Types of Surgery WHISPER VOICE TEST
10. Care of the Client Undergoing Ear Surgery • The examiner covers one ear with the palm of
the hand, then whispers softly2- syllable
DIAGNOSTIC TESTS FOR AUDITORY words from a distance of 1 or 2 feet from the
ACUITY unoccluded ear, and out of the patient's sight
TUNING FORK TESTS / RINNE'S TEST (e.g. thirteen, fourteen, fifteen).
• Compares air conduction from bone • The person with normal hearing acuity can
conduction, differentiates conductive and correctly repeat what was whispered.
sensorineural hearing loss.
• The vibrating tuning fork is placed against AUDIOMETRY
the mastoid bone/behind the ear lobe (bone • It is the single most important diagnostic
conduction); then, it is placed 2 inches from instrument in detecting hearing
the opening of the ear canal (air conduction)
• Interpretation of results is as follows: Types of Audiometry
• Normal: air conduction is better than bone • Pure-tone Audiometry. The louder the tone
conduction (the tone is louder in front of the before the client perceives it, the greater the
ear) hearing loss.
• Conductive hearing loss: bone conduction is • Speech Spokenword is used to determine the
better than air conduction (the tone is louder ability to hear and discriminate sounds and
behind the ear) words. The louder the sound before the client
• Sensorineural hearing loss; same as the perceives it, the greater the hearing loss.
normal finding • Tympanogram or Impedance
• It is more accurate in diagnosing conductive Audiometry. It measures middle ear muscle
hearing loss like in otosclerosis. reflex to sound stimulation and compliance
ofthe tympanic membrane, by changing the
WEBER TEST air pressure in a sealed ear canal. Compliance
• The rounded tip of the handle of the vibrating is impaired with middle ear
tuning fork is placed on the client's head
• Interpretation of results is as follows: OCULOVESTIBULAR TEST/ ICE WATER
CALORIC TEST
• Normal result: lateral conjugate nystagmus • Noise in the ear is a very common
of the eyes away area of stimulation. • Its quality varies from a high-pitched whistle
• Abnormal result: dysconjugate nystagmus to the clanging of bells or recognizable
of the eyes. snatches of
• Then, irrigate the ear with warm CLASSIFICATIONS OF HEARING LOSS
• Normal result: lateral conjugate nystagmus • Conductive hearing. It involves interference
of the eyes toward from the area of with conduction of sound impulses through
• Abnormal result: dysconjugate nystagmus the external auditory canal, the eardrum or
of the eyes the middle ear. It is validated by Rinne's Test
• Sensorineural hearing loss. It results from
• Remember COWS: Cold Opposite Warm
Same disease or trauma to the inner ear or acoustic
nerve. It is validated by Weber's Test.
• WITH HEARING LOSS
• Mixed hearing. It involves both conductive
and sensorineural hearing loss.
SYMPTOMS OF EAR DISEASES
DEAFNESS
ASSESSMENT IN A CLIENT WITH
• Means that the patient has a hearing loss,
which may be mild or severe. HEARING LOSS
• Hearing loss may be conductive, • Irritable, hostile or hypersensitive in
sensorineural or mixed types. interpersonal o Has difficulty in following
• The most common cause of deafness in directions.
childhood is serous otitis media whereas in • Complains about people mumbling.
adults, presbycusis is most common cause. • Turns up volume on
• Presbycusis means deafness of the elderly • Asks for frequent repetition.
and it is a sensorineural hearing loss caused • Answers questions
by the degeneration of the nervous tissue. It • Leans forward to hear better, face looks
is more common among men, over 50 years serious and strained. o Loses sense of humor,
of becomes grim and
• Hearing loss in presbycusis is predominantly • Experiences social
in the higher frequencies (high-pitched • Develops suspicious
sounds like women's voice). • Has abnormal articulation.
• Complains of ringing in the ears.
EAR PAIN • Has unusually soft or loud
• Earache or otalgia is a very common • Dominates
complaint.
• In children, the most common cause is acute GUIDELINES FOR COMMUNICATING
otitis media whereas in adults, it is otitis WITH THE CLIENT WITH HEARING
externa. IMPAIRMENT
• The pain may arise from the ear itself or from • Talk directly facing the person in order to
an adjacent site with a shared nerve supply. allow reading of lip movements.
• The most common site for referred pain is the
• Speak in clearly enunciated words, using
throat, where infections more rarely, normal tone of voice. Do not shout. High-
malignant tumors are responsible.
pitched sound is used when shouting. This is
more difficult to understand especially
VERTIGO
among older people.
• A form of dizziness where the patient
• Use gestures with
experiences a spinning sensation. It is a
common symptom when the balance or • Do not whisper to anybody in front of the
vestibular system of the inner ear is diseased. hearing-impaired client
It is accompanied by nausea and vomiting. • Do not avoid conversation with a person who
has hearing loss
TINNITUS • Do not show annoyance by careless facial
• Move closer to the person or toward the better secretions from special glands in the skin of
ear if he/she does not hear the outer ear.
• Do not smile, do not chew gum or cover the • In most people, the wax escapes as it is
mouth when talking to the person. So the formed but in some, it remains in the ear
person can read the lip movements. canal, obstructing it and causing deafness. o
• Encourage the use of hearing aid if the client • Olive oil or liquid paraffin eardrops or
has hydrogen peroxide will soften the impact
wax, which is then removed by irrigation.
COMMUNICATION WITH HEARING • It is important that the water in the syringe
IMPAIRED PATIENT should be at body temperature so as not to
NONVERBAL AIDS stimulate the inner ear and cause dizziness.
1. Draw attention with hand movements. • The jet of water is directed at the wall of the
2. Avoid covering face and mouth with hands ear canal and the wax is washed out. The ear
3. Avoid chewing, eating, smoking while must be dried gently after the irrigation and it
talking should be examined by a doctor to exclude
4. Maintain eye contact any damage to the tympanic membrane.
5. Avoid distracting environments
6. Avoid careless expression that the patient FOREIGN BODIES
may misinterpret • These are commonly found in the ears of
7. Use touch children and the variety is immense.
8. Move close to the better ear Sometimes they can be removed by a probe
9. Avoid light behind speaker. The patient will or irrigation with warm water but the child is
not be able to see the speaker's face and facial often frightened and uncooperative and a
expressions that will help him understand general anesthetic will be necessary.
what is being communicated • The ear must always be checked to exclude
any underlying damage. o An insect in the ear
VERBAL AIDS is treated similarly to the abovementioned
1. Speak normally and slowly intervention.
2. Do not over exaggerate facial expressions • If the foreign body is a vegetable seed, do not
3. Do not over enunciate irrigate the ear. Vegetable seeds expand when
4. Use simple sentences. exposed to water.
5. Rephrase sentence, use different words
6. Write name or difficult words. OTITIS EXTERNA
7. Avoid shouting • This is an inflammation of the outer ear that
8. Speak in normal voice directly into better ear. is lined by skin. The condition is usually
bilateral and the symptoms start with itching.
DISEASES OF THE OUTER EAR • The patient scratches the ear that becomes
BAT EAR infected, painful and sometimes blocked by a
• The pinna protrudes from the side of the head thin mucopurulent discharge.
because the ridge of the antihelix has not • Allergy, stress and the presence of
formed. The child maybe the object of contaminated water may all play a part but
mockery the treatment is the same.
• The antihelix can be reconstructed fairly • Any precipitating cause is removed and a
easily through an incision on the back of the swab is taken for culture and sensitivity. The
pinna. ear canal is cleaned gently, thoroughly and
frequently using a wisp of cotton wool on the
WAX (IMPACTED CERUMEN) tip of a suitable probe.
• Wax or cerumen is a normal substance • Drops are then instilled directly or used to
produced in the external ear canal. It is made infuse a small wick of ribbon gauze which is
up of epithelial scales mixed with the left in the ear for one or two days. The drops
may be simple disinfectants or may be
 combinations of topical antibiotics (to kill the hole is prevented from healing by inserting a small
bacteria) and steroids (to reduce plastic tube (grommet, dottle or stopple).
inflammation).
• The condition tends to recur. At the same time, any underlying cause (sinusitis or
enlarged adenoids) is treated. As long as the grommet
BOILS remains in place and remains unblocked the hearing
A boil or furuncle is found in the outer hair-bearing is normal.
skin of the ear canal. It is very painful because the
skin at this site is firmly tethered to the underlying However, the grommet drops out after tubes may be
cartilage. Like boils elsewhere, it is caused by the middle ear. The majority of patients with
staphylococcus and the relevant antibiotic is only grommets in place can be allowed to go swimming
necessary when the symptoms are severe. Analgesics although earplugs are advisable. It is hoped that the
are necessary and the possibility of underlying patient will have outgrown the problem by then, but
diabetes must be excluded. a grommet may need to be reinserted if fluid
reaccumulates.
TUMORS
Malignant tumors of the ear are most common in the
outer ear where both basal cell carcinoma and ACUTE OTITIS MEDIA
squamous carcinoma are found. The small lesion is The middle ear is in continuity with the nasopharynx
treated with radiotherapy but the larger will need and is therefore very prone to infection from it. This
surgical excision. is especially so in the presence of serous otitis media
when a convenient culture medium is available for
SEROUS (SECRETORY) OTITIS MEDIA the invading bacteria. The middle ear mucosa
When the Eustachian tube becomes blocked, the air becomes inflamed and the cavity fills with which
trapped in the middle ear is absorbed into the escapes by bursting out through the tympanic
surrounding tissues and is replaced by thin fluid. In membrane into the external ear.
time, small glands appear in the lining of the middle
ear and the mucus which they secrete, explain the The patient, who is usually a child with a cold,
popular name of "glue ears" which is given to this develops an earache of increasing severity that ceases
condition. when the membrane bursts.

It is seen most in those children where an immature The perforation usually heals after 2 to 3 days but this
musculature and repeated upper respiratory tract should be checked after one month and the presence
infections, predispose to tubal obstruction. of an underlying serous otitis media excluded.

The child develops a hearing loss that may pass The patient should be confined to bed and given
unnoticed. However, the parents may have noted that analgesics.
the child's schoolwork has deteriorated or that he
turns up the television. There may also be associated A covered hot water bottle applied to the ear is
episodes of earache caused by a suppurative helpful and warm olive oil drops will soothe the
infection of the fluid. inflamed membrane.

An examination of the ear will reveal the presence of If a patient is seen before the perforation occurs,
fluid behind the tympanic membrane and a simple penicillin should be given and should be continued
whisper test or an audiogram will confirm the for at least 5 days and until the inflammation has
presence of a hearing loss. If the condition is settled.
temporary or intermittent, nothing needs to be done
since most children outgrow the condition. A swab should be taken from the discharging ear and
sent for culture and sensitivity.
If it is more severe, an alternative means of allowing
air into the middle ear, must be found. A hole is made Complications may arise but these are now rare.
in the tympanic membrane (a myringotomy) and the
The most common is acute mastoiditis, a condition forms from an in pouching of the upper
in which an abscess develops in the mastoid bone and segment of the tympanic membrane, into the
burst out behind the ear. middle ear cavity
• Initially, the epithelial scales escape into
It is now only seen in children whose natural defense external canal, but as the mouth of the pouch
mechanisms are not functioning normally. narrow they are retained and accumulate.
• The cholesteatoma is unique that it has the
CHRONIC OTITIS MEDIA property of eroding most of the tissues that
When a middle ear infection becomes persistent it is encounters. The contents of the cyst becomes
called chronic otitis media. infected and the condition may be regarded as
a for of chronic otitis media
Permanent damage is done to the tympanic • The extent of the damage determined by the
membrane and to the ossicles and the patient may be direction in which the cholesteatoma
very deaf with a large central perforation and a enlarges.
persistent discharge. • Usually the ossicles are damaged, but an
upward extension will produce a brain
The discharge is particularly likely to occur when the abscess or meningitis.
patient has a cold because infected secretions pass up • Similarly, a downward extension may
the Eustachian tube. produce a facial paralysis or damage the inner
ear
An attempt is made to remove any source of infection • The treatment will include surgical and some
in the nose or and the local discharge can be form of radical mastoidectomy, which is
controlled by regular irrigation and the instillation of necessary for its removal.
eardrops.
OTOSCLEROSIS
When the ear has been dry for several months it is
• In otosclerosis, abnormal, spongy, highly
suitable for a surgical repair of perforation. • A piece vascularized bone grows across the margins
of fascia is taken from the surface of the temporalis of the oval window and to the footplate of the
muscle and the thin tissue is grafted over the stapes that longer vibrate condition is more
perforation. common in women.
• It begins in early adulthood and the deafness
The graft may be laid on the inner or the outer surface
progressively worsens.
of the tympanic membrane and the operation is
known as a myringoplasty • It causes conductive hearing loss.
• Rinne's test indicates that bone conduction is
Similarly, any loss of ossicular continuity can be better than air conduction
corrected by repositioning a damaged • The treatment is a choice between a hearing
ossicle or by replacing it with a piece of bone or a aid and surgery and the operation is known as
prosthesis. stapedectomy.
• The mobile part of the stapes is removed and
This operation is called tympanoplasty. More hole is made in the fixed footplate.
recently it has become possible to remove the • A Piston (or a similar prosthesis) is placed in
tympanic membrane and its attached ossicles in one the hole and hooked around the incus to
block from a cadaver. reestablish sound transmission.
• The inner ear is at risk during the operation
These homograft tissues can then be implanted into a and this must be clearly explained to the
suitable patient but the operation is technically very patient.
difficult. • Some dizziness almost always occur
temporarily and this is countered by
CHOLESTEATOMA antivertigo drugs.
• This cyst lined by squamous epithelium and
filled with layers of epithelial scales. The cyst
 DISEASES OF THE INNER EAR • Avoid reading during vertigo.
• Any disease affecting the inner ear causes • Provide quiet, darkened room
damage to the delicate nerve endings • Provide soft, mellow music during tinnitus to
responding for hearing and balance and the dived the patient's attention.
patient may complain of vertigo, deafness or • Avoid alcohol, caffeine, tobacco. These
tinnitus. cause exacerbation of symptoms.
• Trauma, loud noises and some drugs may • Stress therapy.
damage the inner ear and they should be
avoided if possible MEDICATIONS
• In Meniere's disease, there is an accumulation • tranquilizers, vagal blockers (atropine),
of endolymph in the inner ear and the patient antihistamines, vasodilators, diuretics
suffers from episodes of severe vertigo. • To reduce vertigo, the following medications
• A tumor known as an acoustic neuroma may may be prescribed:
occur in the internal auditory canal and its o Diazepam (Valium)
symptoms will mimic those of inner ear o Meclizine (Antivert/ Bonamine plus
disease. nicotinic acid)
• The ear, nose and throat surgeon carries out o Fentanyl with Droperidol (lnnovar)
many investigations to distinguish between
these in an attempt to diagnose a neuroma at ACOUSTIC NEUROMA
an early age. A benign tumor of the vestibular or acoustic nerve.
The tumor may cause damage to hearing and to facial
MEINIERE’S DISEASE (ENDOLYMPATIC movements and sensations. Symptoms begin with
HYDROPS) tinnitus and progress to gradual sensorineural
It is characterized by accumulation of endolymph in hearing loss.
the inner ear. It is chronic, with remissions and
exacerbations. Treatment includes surgical removal of the tumor via
craniotomy. Care is taken to preserve the function of
CAUSES the facial nerve. Postop nursing care is similar to post
• Unknown operative craniotomy care.
• Virus
• Emotional Stress An acoustic neuroma expands out of the internal
auditory canal, displacing the cochlear, facial, and
ASSESSMENT IN MENIERE'S DISEASE trigeminal nerves located in the cerebellopontine
• Vertigo (most characteristic manifestation) angle.
• Unilateral or bilateral gradual hearing loss
• "Drop attacks" (the patient experiences the *Note: After surgery, the patient may experience
feeling of being pulled to the ground) asymmetry of the face due to affectation of the facial
• Feeling of as if one is whirling in space nerve. This will spontaneously be resolved in few
• Tinnitus (described as "roar" or "like the months.
ocean")
• Nausea and vomiting There will be dryness of the eye on the affected side
and this eye will not be able to produce tears for
• Weber Test shows that tone lateralizes better
sometime. Artificial tears may be instilled into the
in the good ear.
eye at regular basis to prevent corneal ulceration.
COLLABORATIVE MANAGEMENT FOR
*There will be absent or diminished taste sensation
THE CLIENT WITH MENIERE'S DISEASE
due to affectation of the facial nerve.
• Bed rest during exacerbation.
• Low sodium diet. To prevent retention of
water.
• Avoid drinking large volumes of fluids.
 DIFFERENT TYPES OF SURGERY o This is to prevent vertigo
• Myringoplasty. It involves closure of perforated • Advise patient to seek for supervision when
tympanic membrane. ambulating for the first time, dizziness or
• Tympanoplasty. It involves closure of lightheadedness may occur. This is to prevent
perforated tympanic membrane, if the middle ear falls.
is involved.
• Myringotomy. It involves a simple incision in
the tympanic membrane.
• Ossiculoplasty. It involves ossicular
reconstruction.
• Stapedectomy. It involves surgical removal of
the stape followed by replacement with
prosthesis
• Stapedotomy. It involves use of laser to create a
hole in the footplate of the stapes and prosthesis
is placed in the hole.
• Labyrinthectomy. It involves surgical removal
of the membranous labyrinth through the oval
window or through the mastoid bone.

CARE OF THE CLIENT UNDERGOING EAR

SURGERY
PREOPERATIVE CARE
• Assess for upper respiratory tract infection.
• Shampoo the hair.
• Inform the client that he/she will be under local
anesthesia but sedated during surgery.

POST OPERATIVE CARE

Instructions include the following:
• Lie on the unoperated side.
• Blow nose gently one side at a time, sneeze
or cough with mouth open for 1 week after
surgery.
• Avoid strenuous physical activity like heavy
lifting for 1 week and avoid exercises or
sports for three weeks postop.
• Change cotton ball in ear daily.
• Keep ear dry for6 weeks postop.
• Do not shampoo hair for 1 week
• Protect ear with 2 pieces of cotton (outer
piece saturated with petrolatum)
• Avoid airplane travel for 1 week postop.
• For sensation of ear pressure hold nose, close
mouth and swallow to equalize pressure
• Report any drainage other than slight amount
of bleeding to the physician.
• Avoid reading, watching TV or fast moving
objects for 1 week postop.
 FAR EASTERN UNIVERSITY
Institute of Nursing
A.Y 2021 – 2022 Second Semester

Medical-Surgical Nursing 2
Module 5Care of Clients with Disturbances in Locomotion

OUTLINE BONES
1. Anatomy and Physiology of the Skeletal • Bone is a living tissue surrounded by soft
System tissue with vascular connections
2. Trauma and Injuries • Enclosed by a dense layer of fibrous tissue
a. Sprain called periosteum
b. Strain • Composed of cells, protein matrix, and
c. Dislocation mineral deposits
d. Concussion • includes 206 bones connected by joints
e. Contusion • 14 % of the body’s total weight
f. Fractures • joints are connected by ligaments and
3. Inflammatory Problems cushioned by cartilages
a. Osteoarthritis
• Tendons attached muscles to the bones
b. Rheumatoid arthritis
c. Gouty Arthritis
Bone consists of:
d. Buerger’s Disease
• Organic components
e. Carpal Tunnel Syndrome
o Collagen fibers impart flexibility
4. Developmental Conditions of the Spine
a. Scoliosis • Inorganic minerals
b. Herniated Nucleus Pulposus o Calcium & Phosphorus (give bone its
5. Metabolic Conditions hardness, strength, and rigidity to
a. Osteoporosis resist compressive forces)
6. Malignancy o Magnesium, Potassium, and other
a. Osteogenic sarcoma trace elements (act as "mortar"
bonding the calcium and
ANATOMY AND PHYSIOLOGY OF THE phosphorous)
SKELETAL SYSTEM
FUNCTIONS OF THE SKELETAL SYSTEM Three Layers of a Living Bone
1. Support. Maintains upright posture 1. Periosteum (outside covering)
2. Hematopoiesis. Formation of blood or of 2. Compact bone (hard bone)
blood cells in the living body 3. Spongy bone (bone marrow)
3. Allowing bodily movement. Serve as a lever a. Red marrow - producing red blood
that magnifies speed of movement or force cells which carry oxygen
(long bones are the levers & the axes b. White blood cells - which fight
(fulcrum) are the joints where bones meet infection
4. Protection. Protects the brain and internal c. Platelets - help stop bleeding
organs d. Yellow marrow (at center) - used to
5. Store minerals such as calcium and store fats
phosphorus.
• Calcium: 99% in skeleton; 1% in
teeth and soft tissues
• Phosphorus: 85% in bones; 15%
spread throughout the soft tissues
Functioning Unit of the Bone 2. Calcitonin- decreases levels of calcium in
the blood by increasing the deposition of
calcium in the bones
3. Vitamin D- causes absorption of calcium
from the intestine
• deficiency of Vitamin D, can cause
the body to release large levels of
parathyroid hormone which can lead
to bone weakening

Three types of bone cells: HUMAN SKELETON

1. Osteoblast- found in deeper layer of • Adult skeleton has 206 bones
periosteum and the bone marrow • Babies are born with 270 soft bones until age
• secretes bone matrix thus involved in 20 or 25
bone formation • Trabecular bone loss begin at 30 - 35 yo
2. Osteocytes- found inside the lamellae • Women - 50%
mature bone cells; involved in bone • Men - 30%
maintenance
3. Osteoclasts- found just beneath the Two Main Divisions:
periosteum; multinuclear cells involved in 1. Axial - 80 bones
bone; destruction, resorption & remodeling • consists of bones that form the axis of the
body and support and protect the organs of
the head, neck, and trunk
• Skull, spine, ribs, spine, sternum

2. Appendicular - 126 bones

• composed of bones that anchor the
appendages to the axial skeleton
• Shoulders, pelvis, upper extremities, lower
extremities

AXIAL SKELETAL SYSTEM

1. BONES OF THE SKULL (The Cranium)
a. Frontal bone (1)- conscious thought,
speech, primary motor area
Bone Metabolism b. Parietal bone (2)- body awareness,
1. Osteon- microscopic functioning unit of mature language, taste, primary sensory area
bone which is surrounded by lamellae c. Occipital bone (1)- vision
2. Bone Marrow- vascular tissue located in the d. Temporal bone (2)- hearing, reading
shaft of long bones and flat bones
1. Yellow Marrow– composed mostly of 2. BONES OF THE FACE
fat cells & myelocytes a. orbit (2)
2. Red Marrow– contains immature RBCs b. nasal (2)
c. zygomatic or cheek bone (2)
Hormones d. maxillary bone (2)
1. Parathyroid Hormone- raises levels of e. mandible (1) (chin bone)
calcium in the blood while increasing the
release of calcium from the bone, it increases 3. RIBS
the absorption of calcium from the intestine a. 1st to 7th- True ribs
and makes the kidneys excrete less calcium b. 8th to 12th- false ribs
c. 11th and 12th - Floating ribs
4. STERNUM (BREASTBONE) a. Ilium
a. Manubrium b. Ischium
b. Body or gladiolus c. Pubis
c. Xiphoid process 4. LOWER EXTREMITIES
a. Femur (thigh bone)
5. VERTEBRAL OR SPINAL COLUMN b. Patella (knee cap)
a. Cervical bones (7) c. Tibia (shi bone)
i. Atlas- 1st cervical bone d. Fibula)
ii. Axis- 2nd vertical bone e. Tarsals
b. Thoracic bones (12) f. Metatarsals
c. Lumbar (5)
d. Sacral bones (fused into one)
e. Coccygeal bones (fused into one)

• C3 – Spontaneous breathing
• C5 – Shoulder abduction, shrugging
• C6 – Supination / wrist extension
• C7 – Wrist flexion
• C8 to T1 – Digital abduction & adduction
• T1 to T12 – Accessory respiration &
abdominal muscles
• L1 to L2 – Hip flexion
• L2 to L4 – Hip adduction
• L5 – Dorsiflexion
• S1 to S2 - Plantarflexion

APPENDICULAR SKELETAL SYSTEM

1. BONES OF THE SHOULDER
a. Clavicle (collarbone)
b. Scapula (shoulder bone)
2. UPPER EXTREMITIES
a. Humerus
b. Ulna and radius
c. Metacarpals (palm)
d. Carpals (wrist)
e. Phalanges (proximal, middle, distal)
3. PELVIS (three hip bones which fuse together
when growth is completed)
 TRAUMA AND INJURIES Clinical Manifestation
SPRAIN • Mild- last a few days
• Is an injury to the ligaments around a joint • Moderate- last one to three weeks
• Twisting • Severe- the muscle is torn apart or ruptured,
• Around the ankle bleeding, swelling and bruising around the
muscle
Clinical Manifestation
• Joint pain or muscle pain Symptoms
• Swelling • Swelling, bruising or redness, or open cuts as
• Joint stiffness a consequence of the injury
• Discoloration of the skin, especially bruising • Pain at rest
• Pain when the specific muscle or the joint in
Pain Assessment (OPQRST) relation to that muscle is used
• Onset • Weakness of the muscle or tendons
• Provocation • Inability to use the muscle at all
• Quality
• Radiation DISLOCATION
• Severity • Displacement of a bone from its normal joint
• Time position, contact

Management (RICES) Causes:

• Rest 1. Trauma
• Ice 2. Disease
• Compression 3. Congenital condition
• Elevation
Clinical Manifestation
• Splinting 1. Burning pain to joint
2. Deformity
Management 3. Stiffness and loss of function
• Analgesic and Anti-inflammatory 4. Moderate to severe edema around joint
medications
o Ibuprofen (Motrin and Advil) CONCUSSION
o Naproxen (Aleve or Naprosyn) • is a violent jarring or shaking resulting in
• Brace or cast to reduce motion of the ankle. disturbance of brain function
• Crutches to prevent bearing weight on the
injured ankle Signs & Symptoms:
• Brief loss of consciousness
STRAIN
• Feeling of nausea and vomiting
• Stretching or tearing of muscle • Headache
• Sudden and powerful contraction • Numbness of extremities
• Hamstring and back injuries are among the • Dizziness
most common strains
CONTUSSION
Possible Causes
• a bruise to the brain which causes bleeding
• Running and swelling inside of the brain
• Jumping
• Throwing, lifting a heavy object Signs & Symptoms:
• Lifting in an awkward position. • Increased ICP
• A chronic strain results from prolonged, • Nausea and vomiting
repetitive movement of a muscle • Sensory & motor reflex is affected
Management (for both Contusion and CLASSIFICATION OF BONE FRACTURES
Concussion) Broad Classification of Fractures:
• Assess ABCs (airway, breathing, circulation) 1. Simple (closed) fracture
• With head-injured patients, cervical spine 2. Compound (open fracture)
stabilization is paramount
• For patients who need airway assistance, the Classification of fractures as to patterns:
jaw thrust maneuver is appropriate to 1. Transverse- a fracture that is straight across
maintain cervical spine control a bone
2. Oblique- breaks runs in slanting direction
Level of Consciousness 3. Spiral- break coils around the bone
• Alert – responds to voice
• Lethargic – responds to voice slowly Classification as to appearance
• Obtunded – responds to touch more than 1. Comminuted- bone splintered into
voice fragments
• Stuporous – responds to pain only 2. Impacted- one end of the fractured bone is
forcefully driven into the interior of the other
• Semi Coma – responds inconsistently to pain
3. Compression- vertebra collapses in itself
• Coma – unresponsive to stimulus 4. Depressed fracture- broken bone being
driven inward
FRACTURE 5. Longitudinal fracture- break runs parallel
• A crack or break in the continuity of the bone with bone
• An interruption of a bone’s wholeness 6. Fracture dislocation- fracture is
accompanied by a bone out of a joint
Causes of fracture:
• More stress is placed upon a bone than it is Other types of fractures:
able to absorb such as: 1. Pathologic- results from a diseased bone
o Direct blow or a crushing form 2. Burst- resulting from direct pressure leading
o Twisting force to impaction of the disc
o Powerful muscle contractions 3. Avulsion- a pulling away of a fragment of a
o Fatigue and stress bone by a ligament and its attachment
• Bones weakened by disease or tumors are 4. Greenstick- bone bends without fracturing
subject to pathological fractures across completely
• Age 5. Ping-pong fracture- a type of depressed
• Genetics skull fracture usually seen in young children,
• Gender resembling the indentation that can be
• Diet produced with the finger in a ping-pong ball
• Hormonal Imbalance 6. Blow-out fracture- fracture of the orbital
floor caused by a sudden increase of
Clinical manifestation intraorbital pressure due to traumatic force;
1. Pain (especially at the time of injury) the orbital contents herniate into the
2. Tenderness at the site maxillary sinus
3. Swelling 7. Teardrop fracture- compression fracture of
4. Bleeding from an open wound with the body of a vertebrae with separation of
protrusion of bone ends bone fragments
8. Jefferson’s fracture- fracture of the atlas
Complications (first cervical vertebra)
1. Blood loss 9. Hangman’s fracture- fracture through the
2. Injuries to organs pedicles of the axis (C2) with or without
3. Growth problems subluxation of the second cervical vertebra or
the third
10. Garland fracture- supracondylar fracture of
the humerus
 11. Neer fracture- shoulder and humeral 2. Midshaft
displaced fracture resulting three or more 3. Distal
fragments
12. Colle’s fracture- displacement of the wrist PRINCIPLES OF FRACTURE TREATMENT
joint rests behind its normal anatomic 1. Recognition
position 2. Reduction
13. Galeazzi fracture- fracture of the distal third a. Closed Reduction- manual
of radius with radio-ulnar dislocation manipulation is used
14. Monteggia fracture- fracture of the shaft of b. Open Reduction- done by nails,
the ulna with dislocation of the radial head screws, pins, plates wires or rods
within the elbow joint i. Open Reduction Internal
15. Bennett’s fracture- fracture plus dislocation Fixation (ORIF)
of the metacarpal bone at the base of the ii. Open Reduction External
thumb Fixation (OREF)
16. Femoral fracture- extends from the hip joint 3. Retention- obtaining union of fracture
down to the knee joint fragments
17. Garden’s fracture- femoral neck fracture 4. Restoration of Function (Rehabilitation)
18. Winquist fracture- fracture of the 3rd femur a. Surgery
19. Barton’s fracture- with slight comminution b. Therapy
at fracture site which looks largely like a c. Exercise
butterfly; fracture site has butterfly fragments
20. Bimalleolar fracture- involves the lateral Conservative Management
malleolus at the medial malleolus • Rest for 4-6 wks.
21. Jones fracture- a fracture of the fifth • Ice packs for the 1st 48 hrs. to control
metatarsal swelling then warm treatment
22. March fracture- a fracture of the distal third • Anti-inflammatory (Ibuprofen)
of one of the metatarsals because of recurrent • Elevate extremity to lessen swelling
stress • Pain management
23. Supracondylar fractures of the femur- • Assess for signs of neurovascular problems
above the knee joint; often involve the like pain, absent pulse, paresthesia, pallor,
cartilage surface of the knee joint paralysis
24. Intertrochanteric his fracture- between the
• Exercise– ROM; deep breathing, muscle
greater and lesser trochanter setting
25. Cotton’s fracture (trimalleolar fracture)-
• Traction
consists of fracture of the medial, lateral, and
posterior malleoli of the tibia
STAGES OF BONE HEALING
26. Malgaigne’s fracture- double fracture of the
1. Reactive Stage
pelvic ring causing pelvic instability
a. Hematoma Formation
27. Salter’s fracture- growth plate fractures
28. Pott’s fracture/ Duputren fracture/ Pott’s • After a fracture, macrophages
syndrome- fracture of the fibula including invade the area due to
malleoli of the ankle, resulting in outward hematoma
and backward displacement of the leg while • Edema, inflammation, pain,
foot is fixed; due to inversion injuries massive disruption to the
channels of blood supply and
Classification in relation to the joint a large amount of bleeding
1. Intracapsular- within the capsule from the fracture fragments
2. Extracapsular- outside the capsule causes immediate swelling
3. Intra-articular- in the joint and bruising
• Blood clots (Fracture
Classification as to location Hematoma) are formed after
1. Proximal injury up to 24 hrs
 b. Cellular Proliferation / Collagen • Clavicle- 3-4 weeks
Formation • Metacarpalso 5-6 weeks
• 24 hrs up to 1-2 wks • Humerus- 6 weeks
• The combination of periosteal • Tarsals- 6-8 weeks
elevation and granulation • Radius- 6-13 weeks
tissue containing blood • Tibia- 8-12 weeks
vessels, fibroblast and • Femur- 12 weeks
osteoblast (bone- producing • Fibula- 12-14 weeks
cells) produce collagen
(tensile strength of bone) to ASSESSMENT
form a substance called Classification of soft tissue injury
osteoids forming a bridge • Grade 0- negligible soft tissue injury
across the fractured site
• Grade 1- superficial abrasion/ contusion
2. Reparative Stage • Gade 2- deep contusion from direct trauma
3. Callus Formation • Grade 3- extensive contusion and crush
injury with possible severe muscle injury,
• 2 wks to 1 or 1 ½ months
compartment syndrome
• Minerals are deposited in the
osteoid forming a large mass of
Gustilo and Anderson Classification System
differentiated tissue, bridging the
(Classification of Open Fracture)
fracture gaps called callus
4. Bone Ossification • Type I - Wound less than 1 cm; without
contamination; minimal injury of soft tissue
• 1 ½ months to 4 months
• Type II - Wound between 1 and 10 cm; mild
• Mineral deposition continues and
contamination; extensive soft tissue damage;
produce firmly reunited bone
minimal to moderate crushing component
thus, fracture ends knit together
3. Remodeling • Type III-A - Wound larger than 10 cm;
5. Remodeling severe contamination; severe crushing
component
• 4 months to 1 year or more
• Type III-B - Wound larger than 10 cm;
• When consolidation is
severe contamination; severe loss of tissues
completed, excess cells or
requiring flap advancement or free flap
devitalized tissues are absorbed
• Type III-C - Wound larger than 10 cm;
The primary cancellous bone is
severe contamination; neurovascular injury
remodeled, compact bone is
Requiring repair
being formed and reorganization
of the new bone into its former
Staging of Pressure Sore
structural arrangement is done;
absorption and depositing • Stage I- erythema/ redness
strength and laminae • Stage II- superficial lesion affecting the
epidermis and dermis
HEALING • Stage III- lesion affecting the subcutaneous
Complications of healing tissues
1. Loss of circulation • Stage IV- lesion affecting the muscles
2. Infection exposing the bones
3. Interrupted or improper immobilization • Stage V- extensive lesion extending to the
4. Inadequate fixation cavities and joints
5. Necrosis due to fixation device
6. Metabolic disturbance Goal of Treatment
• Regain and maintain correct position and
Average period for bone healing alignment
• Phalanges- 3 weeks • Regain function of involved part
 • Return client to ADL in the shortest time EXERCISE
Exercise- the active contraction and relaxation of
MANAGEMENT muscles
SURGICAL MANAGEMENT
1. Vertebroplasty- – insertion of a glue-like Passive Exercise- movement of the body usually of
material (methylmethacrylate) into the center the limbs without effort by the patient
of the collapsed spinal vertebra in order to
stabilize and strengthen the crushed bone. Active exercise- movement of the body with effort
The glue is inserted with a needle and syringe of the patient
through anesthetized skin into the midportion 1. Isotonic (dynamic)- muscle tension is
of the vertebra under the guidance of constant
specialized x-ray equipment. Once inserted, - Muscle shortens to produce muscle
the glue soon hardens, forming a cast-like contraction and movement
structure with the locally broken bone. - Size, shape, and strength of the muscles
2. Open Reduction External Fixation and joint mobility are maintained
3. Endoprosthetic replacement - Improves cardiac-respiratory function
4. External fixation device– until bone is - Running, walking, swimming, cycling,
repaired and healed active ROM, pushing or pulling against a
stationary object, pressing the feet
NURSING INTERVENTIONS FOR PATIENTS against a foot board, using trapeze to lift
WITH FRACTURE the body off the bed, lifting buttocks of
1. Comfort the bed by pushing with hands against
2. Adequate oxygen to tissues the mattress, pushing the body to a sitting
3. Rest position
4. Total body mobility while the injured part at 2. Isometric (static/setting)- there is a change
rest on muscle tension but no change in muscle
strength
Complications - No muscle or joint movement occurs
1. Deep vein thrombosis - To strengthen abdominal, gluteal, and
2. Pulmonary embolism quadricep muscles used in ambulation
3. Contractures but are no useful in preventing joint
4. Malunion- bones heal but become crooked contractures because joint movement is
5. Non-union- fractures that never heal absent
6. Carpal tunnel syndrome - Valsalva maneuver
7. Compartment syndrome- a serious condition 3. Isokinetic (resistive)- muscle contraction
that involves increased pressure in a muscle and joint movement
compartment - Person moves or tense against resistance
- Special machines/ devices provide the
SLINGS AND BANDAGES resistance to the movement
• Bandage- are any materials that hold the - Used in physical conditioning
dressing in place, hold pressure on a wound, - To build up certain muscle groups
as a support or to secure a splint-like dressing,
bandages can be bought of improvised Aerobic exercise- the amount of oxygen take into
• Sling- provide support and protection of the the body is greater than or equal to the amount the
arm; can be improvised with a scarf, belt, body requires
necktie, etc. - Improves cardiovascular fitness
• Cast- a protective shell of fiberglass, plastic, - Brisk walking and swimming
or plaster, and bandage that is molded to
protect broken or fractured limb(s) as it heals Anaerobic exercise- activity in which the amount of
oxygen taken into the body is sufficient to meet the
body’s needs
- Oxygen need is made up later
 - To develop muscle tone and to improve
cardio-respiratory function Cast Care
- Running up 3 flights of stairs 1. Do not wet, cut, or heat
2. Allow the cast to dry naturally in circulating
Range of Motion (ROM) Exercise- the totality of air
movement a joint is capable of doing 3. If the cast becomes loose, cracked, and soft,
• Passive ROM- another person moves each of it is no longer keeping the injured body
client’s joints through their complete ROM, immobilized
maximally stretching all muscle groups 4. Do not lush any objects inside the cast
within each plane over each joint to maintain 5. Check the circulation of the finger or toes
joint flexibility 6. Trim rough edges
• Active ROM- isotonic exercise in which the
client moves each joint in the body through Cast Syndrome
its complete ROM, maximally stretching all 1. Impaired venous circulation
muscle groups within each plane, over the a. Swelling
joint b. Pain/ discomfort
o Maintains/ increase muscle strength c. Cyanosis of nail beds
and endurance d. Muscle spasm
o Helps to maintain cardio-respiratory 2. Impaired arterial supply
function in an immobilized client a. Slow capillary refill
o Prevent deterioration of joint 3. Abdominal pressure
capsules, ankylosis, and contractures 4. Feeling of tightness or bloating
• Active-Assistive ROM- client uses a 5. Inability to take deep breaths
stronger opposite arm or leg to move each of
the joints of a limb incapable of active motion Plaster Sore
o Increases active movement on the 1. Burning, itching, or stabbing pain
strong side of the patient’s body 2. Disturbed sleep
o Maintains joint flexibility on the 3. Elevated temperature
weak side (for stroke patients) 4. Heat and swelling of the digits
5. Visible pus or staining of the cast
TREATMENT MODALITIES
• Heat application. Heat pad maybe applied to ASIA Impairment Scale (American Spinal Injury
warm up the muscle prior to doing exercising Association)
and stretching • A (complete): no motor or sensory function
• Cold application. Ice pack after exercise to preserved in S4-S5
soothe the muscles and soft tissues • B (incomplete): there is sensory but no motor
• Transcutaneous Electric Nerve function preserved below the neurological
Stimulation (TENS). Sends a painless level and includes S4-S5
electrical current to specific nerve. The • C (incomplete): motor function is preserved
current maybe delivered intermittently. The below the neurological level, and have a
mild electrical current generates heat that muscle grade less than 3
serves to relieve stiffness, improve mobility, • D (incomplete): motor function is preserved
and relieve pain. It stimulates the body’s below the neurological level, and have a
production of endorphins (natural pain muscle grade of 3 or more
killer). • E (normal): motor and sensory function are
normal
ASSESSMENT
Neurovascular Assessment For Patient With Muscle Grading
Cast • 0- total paralysis
Movement, color, numbness, edema, sensation, • 1- palpable or visible contraction
warmth
 • 2- active movement, full range of motion,
gravity eliminated
• 3- active movement, full range of motion,
against gravity
• 4- active movement, full range of motion,
against gravity, and provides some resistance
• NT- not testable; patient unable to reliably
exert effort or muscle available for testing
due to factors such as immobilization, pain on
effort or contracture

Grading for ADLs

• 0: completely able; activity completed
without modification, within reasonable time
• 1: ability with aids/difficulty; activity
completed with prior preparation or with
assistive devices or aids, or beyond a
reasonable time
• 2: able with helper; activity completed only
with help or assistance of another person, or
under supervision by cuing
o Individuals performs at least half the
effort to complete the activity
• 3: unable; individual assists minimally (less
than half of effort), or is totally dependent
 INFLAMMATORY CONDITIONS DIAGNOSTIC PROCEDURES
OSTEOARTHRITIS Laboratory Examinations for Osteoarthritis
• Breakdown/ tearing or thinning of cartilage 1. Joint fluid analysis- fluid is extracted from
resulting in friction on the ends of the bones the knee with a needle
as they move 2. CBC, C-reactive Protein, ESR
• Is limited to the joints
• Unilateral but becomes symmetrical later Diagnostics for Osteoarthritis
1. X rays- shows narrowing of the space
Synonyms: between the joint (articular surface),
• Osteoarthritis (OA) osteophytes, cyst formation and hardening of
• Degenerative Joint Disease (DJD) the underling bone
• Hypertrophic Arthritis 2. MRI- complex, non-invasive imaging
technique capable of visualizing all structures
Predisposing factors: within the joint
• Over age 40 3. CT scan- provides information on the bony
structures of the joint but in greater detail
• Collagen disturbances
4. Arthroscopy- a tiny camera that can see
inside the joint to diagnose source of pain
o Osteoarthritis
o Rheumatoid arthritis
Four Phases in Osteoarthritis
o Gouty Arthritis
1. Stationary phase- formation of osteophytes
o Buerger’s Disease
(bony outgrowths at the joint margins) and
o Carpal Tunnel Syndrome
joint space narrowing
• Diabetes 2. Obliferation phase- eventually fissures
• Obesity (splitting) and pits (small holes) develop in
• Trauma to the bone the cartilage to increase the surface area to
• Wear and tear (overuse) offload the pressure on that joint by
• Infected joints, chronic gout, and rheumatoid disturbing the weight; thus, joint space is
arthritis, Paget’s disease, unequal leg length obliterated
3. Erosive phase- appearance of subchondral
Body part affected: joints in the spine, hips, knees, cysts (cysts in the bone underneath the
and hands cartilage)
4. Bone repair and remodelling- damaged
CLINICAL MANIFESTATIONS bone attempts to repair itself
• Stiffness or difficulty moving the joints and
in some cases bone spurs (hard lumps) MANAGEMENT
• Commonly occurs in the morning after Goals of Treatment for Osteoarthritis
awakening 1. To control pain
• Lasts only less that 30 minutes 2. To improve joint function
• Decreases with movement, but worsens after 3. To maintain normal body weight
increased weight bearing activity 4. To achieve a healthy lifestyle
• Crepitation may be elicited
• Swelling MEDICAL INTERVENTIONS FOR
• Pain may get worse with overuse and may OSTEOARTHRITIS
occur at night at rest 1. Analgesics/ Painkillers- reduces pain but no
• Heberden’s nodes- abnormal cartilaginous effect on inflammation; acetaminophen
or bony enlargement of a distal inter- 2. Nonsteroidal anti-inflammatory drugs
phalangeal joint of the finger (NSAIDs)- reduce inflammation and pain
• Bouchard’s nodes- abnormal cartilaginous or a. Ibuprofen (Advil, Motrin)
bony enlargement of a proximal b. Naproxen (Aleve)
interphalangeal joint of a finger 3. COX 2 medicines (Celecoxib, Celebrex)
 4. Duloxetine (Cymbalta)- antidepressant; for 3. Disability
chronic musculoskeletal pain (joint and
muscle pain) Prognosis for Osteoarthritis
5. Orthoses- assistive devices to improve Osteoarthritis cannot be cured but early diagnosis
movable body parts or to support, align, and treatment can help to reduce symptoms and
prevent, or correct deformities minimize complications
a. Splints or braces- joint alignment and
weight distribution RHEUMATOID ARTHRITIS
b. Walkers, crutches or canes, and • An autoimmune disease in which the body’s
orthopedic footwear immune system attacks itself
• Involves numerous types, including
SURGICAL INTERVENTIONS FOR OA macrophages, T-cells, B-cells, fibroblasts,
1. Arthroscopy- examination of the inside of a chondrocytes, and dendritic cells
joint using a small camera (endoscope) • Rheuma- humorous substance that flow
2. Arthroplasty- repair of a joint in which the through the body the come to stop in certain
joint surfaces are replaced with artificial parts of the body, causing pain and swelling
materials, usually metal or plastic
3. Osteotomy- incision or cutting the bone Body parts affected in rheumatoid arthritis:
4. Chondroplasty- surgical repair of the • Joints on both sides of the body equally
cartilage affected
5. Arthrodesis- surgical fusion of the bony • Wrists, fingers, knees, feet, and ankle
ends of a joint preventing joint movement
6. Joint replacement- removal of diseased or Predisposing factors
damaged bony ends and replacement with a 1. Age: 40-50 years old
man-made joint composed of a combination 2. Gender: women more than men
of mental and plastic 3. Genes
7. Tidal irrigation- introduction of large
volume of saline into the joint through Precipitating Factors
cannulas and the removal of this fluid 1. Infection
2. Hormone changes
NURSING INTERVENTIONS FOR 3. Smokers
OSTEOARTHRITIS 4. Rheumatoid factor
1. Weight loss
2. Diet CLINICAL MANIFESTATIONS
a. Supplements of antioxidants 1. Attacks multiple joints simultaneously and
b. Vitamin E symmetrically
c. Vitamin D (400 IU) 2. Usually hands and other joints like hips are
d. Calcium (1000-1200 mg) affected
3. Regular exercise to help strengthen the 3. Pain & stiffness worse in the morning
muscles and potentially stimulate cartilage 4. Sjogren Syndrome
growth a. Dry mouth (xerostomia)
4. Avoid high-impact sports b. Dry eyes (keratoconjunctivitis sicca)
5. Hot soaks and warm wax (paraffin) c. Dry vagina
6. Orthoses: splints, braces, walkers, crutches, 5. Swan neck deformity- flexion of the distal
or canes, and orthopedic footwear to support, inter-phalangeal joint and hyperextension of
align, prevent, or correct deformities the proximal inter-phalangeal joint
7. Physical therapy 6. Boutonniere Deformity- flexion of the
8. Occupational therapy proximal inter- phalangeal joint with hyper-
extension of the distal inter-phalangeal joint
Complications of the finger
1. Joint damage
2. Deformity
 7. Pannus- vascularized granulation tissue rich 5. Antinuclear Antibody (ANA)- substances
in fibroblasts, lymphocytes and macrophages produced by the immune system that attack
derived from synovial tissue, overgrows the the body's own tissues
bearing surface of the joint • Low titers are in the range of 1:40 to
1:60
Classification of Severity of RA 6. Serological Point–of-Care Test (POCT)-
1. Stage I- no damage seen on x-ray, though for early detection of RA
there may be signs of thinning 7. Ferritin levels- Ferritin is a blood cell
2. Stage II - on x-ray, with evidence of bone protein that contains iron
thinning around a joint with or without • Normal range: Increased in arthritis:
slight bone damage joint mobility may be Men = 24 to 336 mcg/liter (iu);
limited atrophy of adjacent muscles Female = 11 to 307 mcg/l (iu)
3. Stage III- on x-ray, evidence of cartilage 8. Anti-Citrullinated Protein Antibodies
and bone damage and bone thinning around (ACPA)- present in many cases even before
the joint onset of disease
• Joint deformity without permanent 9. Liver enzyme test- elevated alanine amino-
stiffening or fixation of the joint transferase (ALT), aspartate
• Extensive muscle atrophy aminotransferase (AST) and possibly the
4. Stage IV- on x-ray, evidence of cartilage & bilirubin connotes inflammation of hepatic
damage & osteoporosis around joint cells
• Joint deformity without permanent 10. Renal function test
stiffening or fixation of the joint
• Extensive muscle atrophy Diagnostics Examinations for RA
1. X-ray- demonstrate juxta-articular
Functional Status of Patients with RA osteopenia, soft tissue swelling and loss of
• Class I- completely able to perform usual joint space, bony erosions and subluxation
ADLs 2. Color & Power Doppler Ultrasound- show
• Class II- able to perform usual self-care and vascular signals of active synovitis
work activities but limited in activities
outside of work (playing sports, household The goal of treatment for RA:
chores) 1. Alleviate current symptoms
• Class III- able to perform usual self-care 2. Prevent future destruction of joints resulting
activities but limited in work and other to handicap if left unchecked
activities
• Class IV- limited in ability to perform usual MANAGEMENT
self-care, work and other activities MEDICAL INTERVENTIONS FOR
RHEUMATOID ARTHRITIS
DIAGNOSTIC PROCEDURES 1. Disease-Modifying Antirheumatic Drugs
Laboratory Examinations for RA (DMARDs)- needs frequent blood tests
1. Rheumatoid Factor- during the first year of a. Methotrexate (Rheumatrex)
illness, rheumatoid factor is more likely to be b. Leflunomide (Arava)
negative with some individuals converting to c. Sulfasalazine
seropositive status overtime 2. Analgesics
2. Complete Blood Count 3. Antimalarial medications- used along with
3. C-Reactive Protein- appears in higher Methotrexate; for pain & inflammation
amounts when there's swelling a. Hydroxychloroquine (Plaquenil)
• Normal is 2- 4.9mg/L b. Sulfasalazine (Azulfidine)
4. Corticosteroids- to reduce joint swelling and
4. Erythrocyte Sedimentation Rate (ESR)-
measure of the presence and severity of inflammation; with long-term side effects;
thus, should be taken; only for a short time
inflammatory and other morbid processes
and in low doses
• Normal is 0-10mm
5. Anti-inflammatory agents
 a. Aspirin COMPLICATIONS OF RA
b. Non Steroidal Anti-Inflammatory 1. Damage to the lung tissue (rheumatoid lung)
Drugs (NSAIDs); can cause stomach 2. Increased risk of hardening of the arteries
problems 3. Spinal injury when the neck bones become
i. Ibuprofen damaged
ii. Naprosen. 4. Inflammation of the blood vessels
iii. Celecoxib (Celebrex) (rheumatoid vasculitis)
5. Swelling and inflammation of the heart
SURGICAL INTERVENTIONS FOR RA (pericarditis) and of the heart muscle
1. Synovectomy- removal of the joint lining (myocarditis), which can lead to congestive
2. Arthroscopic or Open synovectomy- heart failure
removal of the inflamed synovia & prevents
a quick destruction of affected joints GOUTY ARTHRITIS
3. Total joint replacement • a chronic, progressive disease caused by an
overload of uric acid in the body, resulting in
NURSING INTERVENTIONS FOR painful arthritic attacks and deposits of lumps
RHEUMATOID ARTHRITIS of uric acid crystals in body tissues
1. Three types of exercises: • Synonyms: “King’s disease” and “Rich
a. Range-of-motion exercises- helps man’s disease”
maintain usual joint movement and
relieve stiffness; helps uphold or Predisposing Factors for Gout
increase flexibility • More common in men
b. Strengthening exercises- help keep • Puberty with peak age of 75
or augment muscle strength
c. Aerobic or endurance exercises- Precipitating Factors for Gout
perks up cardiovascular fitness; help • High purine diet (meat, seafoods)
control weight and improve overall • Obesity
function
• High blood pressure
2. Special tools to improve hand movements
• Leukemia, Lymphomas, Lead poisoning
(e.g. special tin openers)
3. Splints or orthotic devices • Menopause
4. Occupational therapy • Moderate to heavy alcohol intake
5. Physiotherapy • Diuretics, Aspirin, Pyrazinamide,
6. Immunoadsorption therapy Ethambutol, Cyclosporine,
7. Joint protection techniques Chemotherapeutic Drugs
8. 8 to 10 hours of sleep per night • Chronic kidney problems
9. Deep heat or electrical treatment
CLINICAL MANIFESTATIONS FOR GOUT
PROGNOSIS FOR RHEUMATOID 1. Nighttime attack of sharp pain in the
ARTHRITIS affected joint (big toe then ankles and
• No known prevention knees are the next) followed by warmth,
• Early treatmentà decreased joint pain and swelling, reddish discoloration, and
damage marked tenderness
• RA at young ages à gets worse more 2. Attacks one joint at a time
3. Tophi- a nodular masses of uric acid
quickly
crystals commonly found as hard nodules
• No proper treatment à permanent joint
around the fingers, at the tips of the
damage
elbows, in the ears, and around the big toe
• No known cure for RA, but many different (Podagra)
types of treatment can alleviate symptoms
and/or modify the disease process
 DIAGNOSTIC PROCEDURES MEDICAL INTERVENTION FOR GOUT
Laboratory Examination: 1. Analgesics
• Uric acid levels in blood test a. Acetaminophen (Tylenol)
• CBC, ESR, CRP 2. Anti-inflammatory agents
a. NSAIDS
Diagnostic Examinations: i. Indomethacin (Indocin)
1. X-rays- to show tophi-crystal deposits and ii. Naproxen (Naprosyn)
bone damage b. Corticosteroids (Prednisone)
2. Arthrocentesis- aspiration of fluid from the 3. Treat elevated levels of uric acid in the
inflamed joint to analyze for uric acid blood
crystals & Infection a. Probenecid (Benemid)- used to
increase excretion of uric acid into
Phases of Gout the urine
1. First stage: Asymptomatic Hyperuricemia b. Allopurinol- prevents uric acid
• The uric acid level in the blood is higher production; blocks the metabolic
than normal, but there are no symptoms conversion from purines in foods to
of gout uric acid
2. Second stage: Acute Gout
• Hyperuricemia has caused the deposit of
uric acid crystals in joint spaces and leads Surgical Intervention for Gout: Excision of tophi
to a sudden onset of intense pain and
swelling of joints NURSING INTERVENTION FOR GOUT
• Commonly occurs at night 1. Weight reduction- reduce dietary fat &
calorie intake with a regular aerobic
3. Third stage: Intercortical or Interval gout exercise program
• Uric acid crystals begin to form in the 2. Dietary changes- shellfish and organ meats
joint fluid and the body often responds such as liver, brains, kidneys, sweetbreads
with a sudden inflammatory reaction: a (high purine)
gout attack • Cherries and an herb called devil's
• Acute episodes separated by periods claw are folk medicine remedies that
without symptoms within days until the have been used as anti-
next attack, usually within 2 years inflammatories
3. Folic acid- may be helpful in inhibiting
4. Fourth Stage: Chronic Tophaceous Gout the enzyme needed to produce uric acid
4. Maintain adequate fluid intake
• Enough uric acid crystals have
accumulated in the body to form gritty 5. Reduce alcohol consumption
nodules called tophi • Alcohol impedes or slow down the
excretion of uric acid from the
• Symptoms may become ongoing
(chronic) and frequently affect more than kidneys
one joint • Causes dehydration which
• There may no longer be periods of time contributes to precipitation of uric
between attacks acid crystals in the joints
• Beer has high purine
MANAGEMENT 6. Avoid aspirin-containing medication -
Goal of Treatment: aspirin prevents kidney excretion of uric
1. To reduce pain and inflammation acid
2. Prevention of future gout attacks 7. Rest the affected joint until the attack
3. Reduce disability quickly and safely ceases & for 24 hours after the attack
4. Prevention of long-term complications, such 8. Elevate painful joints
as joint destruction and kidney damage 9. Follow a moderate exercise program
 BUERGER’S DISEASE CLINICAL MANIFESTATIONS
• It is an obliterative disease of arteries and Triad of symptoms and signs:
veins characterized by acute and chronic 1. Digital arteries occlusion- decrease in the
inflammation in the blood vessels of the blood supply (arterial ischemia/Diminished
lower and upper extremities which begins in distal pulses)
the small arteries and progresses to 2. Raynaud’s phenomenon / Claudication-
• the larger vessels that result in thrombus Distal extremities (fingers, toes, hands, feet)
formation and occlusion of the vessels turn cold, white, blue then intense rubor upon
• It is an autoimmune reaction (body’s immune exposure to cold.
system attacks body’s own tissue) triggered 3. Pain- it is induced by insufficient blood flow
by tobacco use during exercise or physical exertion and cold
• Buerger's disease was first reported by Felix temperatures which typically begins in the
Von Winiwater in 1879 in Germany legs or gastrocnemius muscle often located in
• It was described in detail by Dr. Leo Buerger the arch of the foot. Pain is relieved by rest or
in 1908 in New York, who called it Presenile if client returns to room temperature
Spontaneous
• Gangrene after studying amputations in 11 Other Signs and Symptoms
patients 1. Superficial (near the skin surface) phlebitis
2. Edema
Synonyms: 3. Erythema, tenderness and warmth
• Thromboangiitis Obliterans (TAO) 4. Gangrene
5. Thick malformed ails
• Vaso occlusive Disease
6. Atrophy of extremities
• Presenile Spontaneous Gangrene 7. Non-healing wound
• Critical Limb Ischemia 8. Numbness
• Corkscrew Collaterals 9. Homan’s sign
• Distal Ischemic Rest Pain
• Ischemic Ulcerations DIAGNOSTIC PROCEDURES
Laboratory Tests
Predisposing Factors 1. Complete Blood Count with differential
1. Race: Buerger disease is relatively less Count
common in people of northern European 2. Erythrocyte Sedimentation Rate (ESR)
descent. Natives of India, Korea, and Japan, 3. Liver Function Tests
and Israel have the highest incidence of the 4. Fasting Blood Glucose
disease 5. C – Reactive Protein
2. Sex: More common in males (male-to- 6. Rheumatoid Factor
female ratio, 3:1) 7. Renal Function Tests
3. Age: 20-45 years 8. Urinalysis
9. Antinuclear Antibody- measures the pattern
Precipitating Factors and amount of autoantibody which can attack
1. Current (or recent) history of tobacco use the body's tissues
2. Presence of distal extremity ischemia 10. Antiphospholipid Antibodies- tests for
• indicated by claudication, pain at rest, presence of proteins in the blood which can
ischemic ulcers or gangrene increase risk for blood clots or pregnancy
• documented by noninvasive vascular losses
testing such as ultrasound
3. Diabetes Diagnostic Tests
4. Hypertension 1. History
5. High cholesterol levels a. Age younger than 45 years
b. Current (or recent) history of tobacco
use
 c. Presence of distal extremity ischemia - to treat scleroderma, Raynaud’s
(indicated by claudication, pain at phenomenon
rest, ischemic ulcers or gangrene) - to slow progressive tissue loss and
(documented by noninvasive vascular reduce the need for amputation during
testing such as ultrasound) the period when they first discontinue
2. Allen’s Test- used to test blood supply to the cigarette smoking
hand specifically, the patency of the radial 3. Vasodilators
and ulnar arteries 4. Vitamins
3. Homan’s sign- a sign of deep vein 5. Calcium Channel blockers
thrombosis (DVT). Positive sign is present 6. Phentofylline - decreases blood viscosity that
when there is pain in the calf on dorsiflexion prevents further thrombus formation
of patient's foot at the ankle while the knee is 7. NSAIDS, preferably Aspirin - thinning of the
fully extended blood with aspirin, etc. to prevent clots have
not proven effective
Imaging Tests 8. Antibiotics
1. Arteriography 9. Analgesics
2. Digital Subtraction Angiography - 10. Anti-inflammatory Drugs - steroids have not
computer-assisted x-ray technique that been shown to be beneficial
subtracts images of bone and soft tissue to
permit viewing SURGICAL MANAGEMENT
a. of the cardiovascular 1. Arteriography- examination of the arteries
system using x-rays following injection of a radiopaque
2. Plethysmography- used to substance
measure changes in volume in 2. Artificial AV fistula
different parts of the body to 3. Lumbar sympathectomy - cutting the nerves
check for blood clots in the to the area to control pain
a. arms and legs 4. Spinal Cord Stimulator Implantation- a
3. Duplex Scanning- a non invasive device used to exert pulsed electrical signals to
procedure using ultrasound to assess the the spinal cord to control chronic pain
blood flow of the body's arteries & veins; 5. Autologous vein Bypass- to improve distal
obtains an image of the carotid artery being arterial flow in patients
studied 6. Omental Transfer
4. Arteriography of extremity - a special dye 7. Angioplasty - a procedure to open narrowed/
is injected into an artery, after which patient blocked blood vessels that supply blood to the
undergo X-rays or other imaging tests legs
5. Doppler Ultrasound of extremity 8. Atherectomy
6. Biopsy of the blood vessel 9. Sympathectomy - cutting the nerves to the area
to control pain
MANAGEMENT 10. Stent Placement - wire mesh stainless steel
There is no cure. tube to hold an artery open to keep it from
• Goal of treatment is to control symptoms closing again
• Immediate and absolute cessation of tobacco 11. Amputation
use
• Early and aggressive treatment injuries to NURSING MANAGEMENT
protect against infections 1. Cessation of tobacco, cigarette, or any
nicotine replacement
MEDICAL MANAGEMENT 2. Gently massage and warm patient to increase
1. Thrombolytics - to lyse already formed circulation
blood clots where ischemia may be fatal 3. Avoid conditions that reduce circulation to
2. Intravenous ILOPROST the extremities
a. cold temperatures
b. use of vasoconstrictors
 c. use of tight or restrictive clothing 2. May be associated with other diseases:
arthritis, hypothyroidism, pregnancy,
4. Avoid sitting or standing in one position for diabetes or other metabolic disorders
long periods of time 3. Edema from trauma which can compress
5. Regular exercise to lose weight if obese median nerve
6. Adequate hydration 4. Obesity
7. Hygiene 5. Intake of caffeine, tobacco smoking
8. Low cholesterol Low salt diet
9. Protect against cold weather Predisposing Factors
10. Keep hands and feet warm 1. Adults age 40-60 years old
11. Avoid walking barefoot 2. Women more than men
12. Use well-fitting protective footwear 3. Acromegaly
13. Protect against infections
CLINICAL MANIFESTATION
Complications 1. Drop objects more than usual
1. Ulcerations 2. Have trouble grasping or pinching objects
2. Gangrene 3. Have trouble using your hands for certain
3. Infection tasks, such as buttoning a shirt, handwriting,
4. Need for Amputation or opening a jar lid
5. Rare occlusion of coronary, renal, splenic, or 4. The muscles at the base of your thumb are
mesenteric arteries smaller and weaker (atrophy) than they used
to be (Thenal Eminence)
Prognosis 5. Cold intolerance
1. Symptoms of thromboangiitis obliterans may 6. Pain, tingling, and numbness in the thumb,
disappear if the person stops tobacco use index, middle, or ring fingers, or tingling in
2. For some, amputation is unavoidable the entire hand
7. Pain that shoots from the hand up the arm as
CARPAL TUNNEL SYNDROME far as the shoulder
• A disorder caused by compression at the 8. A swollen sensation in your fingers, even
wrist, of the median nerve supplying the though they may not be visibly swollen
hand, causing numbness and tingling 9. Symptoms are worse at night after strenuous
• At the base of the palm is a tight canal or activity
“tunnel” through which tendons and nerves 10. Hands feel weak in the morning
must pass
• Median Nerve- narrow passage between the • Early diagnosis and treatment are important
forearm and hand to avoid permanent damage to the median
• “The Carpal Tunnel” is an entrapment nerve
neuropathy that occurs when the median • A physical examination of the hands, arms,
nerve at the wrist is compressed by a shoulders, and neck can help determine if
thickened flexor tendon sheath, skeletal the patient's complaints are related to daily
encroachment, edema or a soft tissue mass activities or to an underlying disorder
• CTS may develop spontaneously without a
known cause, or may result from disease or DIAGNOSTIC TESTS
injury 1. Tinel’s Sign. The doctor will gently tap the
front of your wrist to see if you feel tingling
Precipitating Factors or pain in your hand or forearm
1. Repetitive activities- those who do repetitive 2. Phalen's Test. The doctor will ask you to
movement more than 6 hours per day are at bend your wrist down as far as it will go and
risk hold this position up to 3 minutes to see if
you feel tingling or pain
3. Nerve conduction test- performed to
evaluate nerve function; measures the nerve's
 ability to send electrical impulses to the hand
muscles, to see if the electrical impulses slow
down the carpal tunnel

MANAGEMENT
MEDICAL MANAGEMENT
1. Rest Splint worn during the day to prevent
hyperextension & prolonged flexion of the
wrist
2. Use of Ergonomic changes at work to reduce
wrist strain (avoidance of repetitive flexion of
the wrist
3. NSAIDs
4. Carpal Canal Cortisone injections to relieve
the symptoms
5. Yoga postures, relaxation & acupuncture to
provide non-traditional alternatives to relieve
CTS

SURGICAL MANAGEMENT
(surgery is recommended if symptoms last over 6
months)
Traditional or endoscopic laser surgical release of
the transverse carpal ligament
1. To perform a carpal tunnel release, the
surgeon makes an incision in the palm of the
hand, above the area of the carpal tunnel
2. The carpal ligament going across the hand is
severed releasing pressure on the median
nerve
3. The patient wears a hand splint after surgery
& limits hand use during healing
4. Full recovery of motor & sensory function
after nerve release surgery may take several
weeks or months

NURSING INTERVENTIONS
1. Assist patient with personal care & ADLs
2. Exercise

PROGNOSIS
• Generally, Recurrence of Carpal Tunnel
Syndrome is rare.
• The majority of patients recover completely