Pulmonary Embolism

Sudden occlusion of a pulmonary artery

Thromboemboli, fat, bone marrow, amniotic fluid, air, foreign substance

DVT most common cause

90% of fatalities occur within 1-2 hours

PE

Pathophysiology

>95% from thrombosis of deep veins

Stasis of blood flow, damage to the vessel wall, alteration in coagulation

Risk factors:

Immobility

Hip/femur fractures

MI, CHF, A Fib

Use of oral contraceptives + smoking

Pregnancy, child birth

Cancer

PE

Manifestations and Complications

Small emboli may be asymptomatic

Symptoms develop abruptly

Dyspnea and pleuritic chest pain, anxiety

Cough (hemoptysis), diaphoresis, tachycardia, tachypnea

Fat emboli

Same as above, along with petechiae

Pulmonary infarct/sudden death

Less than 10%

PE

Collaborative Care

PREVENTION

Early ambulation after surgery

SCDs, TED hose

Active and passive leg exercises

O2 therapy, analgesics

PE

Pharmacology

Anticoagulation therapy

Heparin: Subq- prophylactic

IV- with known PE

LMW Heparin (Lovenox)

Coumadin

Takes 5-7 days to become effective

Fibrinolytic therapy

Restore pulmonary blood flow, reduces pulmonary artery and Rt heart pressures

PE

Surgery

Device inserted to trap large emboli while allowing blood flow through the inferior vena cava

Greenfield filter

Umbrella filter

Still require anticoagulation

PE

Nursing Care

Early ambulation

SCDs, Ted hose

Leg exercise

No pillows under knees or raised knees

Monitor patient

LOC, O2, ABGs, vasopressors, VS, cardiac monitor, Lab tests

Accumulation of air in pleural space

Integrity of the visceral or pleural space is lost and air enters equalizing the negative pressure

Natural recoil causes the lung to collapse to a degree depending on how much air accumulates in the space

Pneumothorax

Spontaneous/Closed

Rupture of an air-filled bleb on the lung surface allowing air to enter the space

Once pressures equalize the lung collapses

Primary

Often affecting tall, slender men between 20-40

Secondary

Overdistension and rupture of alveolus

COPD, asthma, ARDS, CF

S&S- Pleuritic chest pain, SOB, increase RR, hyperresonant to percussion, diminished/absent breath sounds

Injury to chest wall

Blunt- MVA, fall, CPR

Penetrating- Stab, GSW, impalement

Open pneumothorax

Air moves freely between pleural space and atmosphere

S&S-Pain and dyspnea, tachycardia and tachypnea

Injury to chest wall or lungs allows air to enter pleural space but not escape

Air accumulates with each breath

Thoracic organs shift to the unaffected side

Ventilation severely compromised

Venous return to the heart compromised

S&S- hypotension, distended neck veins, tracheal shift, possible signs of shock

Pneumothorax

Nursing Care/Home Care

Impaired gas exchange

Risk for injury

Recurrence following spontaneous pneumo is 50%

Limit exposure to high altitudes, flying in unpressurized aircraft, or scuba diving

Teach S&S

Blood in pleural space

Usually results from trauma or surgery

Pressure on affected side impairs ventilation and gas exchange

Rapid versus slow accumulation

Diminished lung sounds, percussion reveals…

Autotransfusion may be necessary

May lead to shock

Simple rib fracture most common

Heals without complications usually

Could lead to pneumonia, atelectasis, respiratory failure

Pneumothorax or hemothorax

Pain on inspiration and coughing

Rapid, shallow respirations

Due to multiple rib fractures resulting in free floating segment of the chest wall

Segment is sucked inward on inspiration and moves outward on expiration

Impairs lung expansion, increases work of breathing

Dyspneic, inspiratory pain, crepitus

ARF

Nursing Care

Inability to sustain spontaneous ventilation

Ineffective airway clearance

Risk for injury

Anxiety

Powerlessness

Defining Criteria

Acute Onset

PaO2/FiO2 ratio < 200 mmHg

Bilateral pulmonary infiltrates

PCWP < 18 mmHg

ARDS

Risk Factors

ARDS

Pathophysiology

Acute lung injury

Systemic inflammatory response

Release of mediators

Microvascular injury

Increased capillary permeability

Alveolar flooding

Pulmonary edema

Alveolar collapse

Profound hypoxemia

Pulmonary hypertension

Alveolar thickening

Pulmonary fibrosis

ARDS

Four characteristics

Permeability defect

Changes in airway diameter

Injury to pulmonary circulation

Disruption in systemic oxygen transport and utilization

ARDS

Exudative Phase

Damage to pulmonary capillary membrane

Interstitial and alveolar edema

Destruction of Type I alveolar epithelial cells

Microemboli are present within the vasculature

ARDS

Proliferative Phase

Continued destruction of Type I cells in addition to Type II cells.

Hyperplasia

Vasculature hypertrophy

ARDS

Fibrotic Phase

Three weeks from onset

Interstitial fibrosis, PHTN

ARDS

Initial Presentation

Tachycardic

Breath sounds clear

Normal chest x-ray

Dyspnea

Respiratory alkalosis

Decreased PaCO2

Normal PaO2

ARDS

Progressive S&S

Tachycardia leads to bradycardia

Crackles and wheezes

Diffuse infiltrates

Dyspnea, fatigue

Metabolic acidosis

Increased PaCO2

PaO2 < 40 mmHg

Shunt 20-30%

ARDS

Nursing Diagnoses

Impaired gas exchange

Ineffective breathing pattern

Risk for infection

Altered nutrition: less than

Anxiety/Pain

Goals of Management

Maximize pulmonary gas exchange

Promote adequate oxygen delivery to tissues

Prevent further injury while treating precipitating cause

ARDS

Six P’s of Supportive Therapy

PEEP

Prevention

Pump

Pipes

Paralysis

Position

Increases end-expiratory volume

Reduces intrapulmonary shunt

Improves lung compliance

Allows for use of lower FiO2

Positive pressure

Pressure controlled

Pressure controlled-inverse ratio

High-frequency jet

Experimental

Extracorporeal membrane oxygenation

Nitric Oxide

Partial liquid ventilation

ARDS

Fluids: To give or not

ARDS alone: fluid restrict

In presence of MODS/SIRS: fluid load

ARDS

Pharmacologic Therapy

Nutrition

Antibiotics

Vasodilators

Steroids

Neutrophil elastase inhibitor

ARDS

Monitor for complications

Secondary infection

Sepsis/SIRS

Shock

MODS

Renal failure

DIC

A type of blood vessel disorder that is included in the general category of atherosclerosis

Begins as soft deposits of fat that harden with age

Referred to as "hardening of arteries"

Can occur in any artery in the body

Atheromas (fatty deposits)

Preference for the coronary arteries

CAD and ACS

Pathophysiology

Atherosclerosis is the major cause of CAD

Focal deposit of cholesterol and lipid, within the intimal wall of the artery

Endothelial lining altered as a result of inflammation and injury

Increase is C-reactive protein (CRP)

Inflammation, triggers rupture of plaques

Fatty streaks

Fibrous plaques

Complicated lesion

Development of Collateral Circulation

Nonmodifiable risk factors

Age, Gender

Ethnicity, Family history

Genetic predisposition,

Modifiable risk factors

Elevated serum lipids, Hypertension

Tobacco use, Physical inactivity

Obesity, Diabetes, Metabolic syndrome,

Psychologic states, Homocysteine level

CAD

Risk Factor Management

Physical activity

Diet, Less than 30% fat intake

Smoking

Decreases HDL, increases LDL, increase blood viscosity

HTN, Control below 140/90 (135/85)

Diabetes, Accelerates the process of atherosclerosis

Drugs

Give ASA, Lipid lowering agents

Estrogen replacement is now in question

Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death

Necrosis of entire thickness of myocardium takes 6 hours

Degree of altered function depends on size and location of MI

MI

Clinical Manifestations

Pain

Total occlusion → anaerobic metabolism and lactic acid production. Described as heaviness, constriction, tightness, burning, pressure, or crushing

Common locations: substernal, retrosternal, or epigastric areas; pain may radiate

MI

Clinical Manifestations

Sympathetic nervous system stimulation results in

Release of glycogen

Diaphoresis

Vasoconstriction of peripheral blood vessels

Skin: ashen, clammy, and/or cool to touch

Nausea and vomiting

Can result from reflex stimulation of the vomiting center by the severe pain

Fever

Systemic manifestation of the inflammatory process caused by cell death

MI

Fibrinolytic therapy

Shock

Underlying Problem

Inadequate tissue perfusion

Leads to microcirculatory failure and ultimately organ failure

Hypovolemic- volume

Cardiogenic- pump

Distributive- plumbing

External

GI losses, Loss of limb

Vessel disruption, Diabetes Insipidus

DKA, Burns, Trauma

Internal

Dissecting aorta, Retroperitoneal bleed

Hemothorax, Splenic rupture

Third spacing

> 40% muscle mass loss (80% of pts)

Papillary muscle rupture

Cardiac Tamponade

Tachyarrhythmias

Bradyarrhythmias

Drugs

Anaphylactic

Neurogenic

Septic

Systemic allergic reaction

Drugs

Food

Insect bites or stings

chemicals

Damage or dysfunction of the sympathetic nervous system

Spinal cord injury

T5 and above

Head injury

Anesthesia

Release of inflammatory mediators that result in massive vasodilation

E coli

Klebsiella

Pseudomonas

Staph aureus

Candida

Anaerobic metabolism only

Decrease in ATP (2 moles versus 36 moles)

Increase in lactic acid

Failure of sodium-potassium pump

Endothelial cells swell, decreasing blood flow

Fluid begins to leak from blood vessels to tissues (third-spacing)

Cell autolyses with release of vasoactive metabolites and phagocytic enzymes

Compensatory (Initial)

Decompensated (Progressive)

Refractory (Irreversible)

Catecholamines released

Systemic venous constriction

Systemic artery constriction

Constriction of precapillary sphincters

Compensated Shock

Clinical Presentations

Anxiety, fear

Thirst

Tachycardia (> 100)

Tachypnea (20-30)

Cool, pale clammy skin

Narrowing pulse pressure

Disappearance of peripheral veins (hands and feet)

Decreased bowel sounds

Urine output <0.5ml/kg/hr

Restlessness, confusion

Blood flow to vital organs reduced

Decreased O2 delivery and/or uptake

Cerebral and myocardial ischemia

Increased lactic acid

Precapillary dilation- edema

Ischemia of tissues

Decompensated Shock

Clinical Presentations

Nausea

Chest pain

Dyspnea (30-40)

Tachycardia (>120)

Hypotension

Cardiac rhythm changes

Mottled skin, peripheral cyanosis

Absent bowel sounds

Anuria (< 15ml/hr)

Agitation…lethargy… coma

Profound hypotension, refractory to therapy

Leaky, porous capillaries

Passive dilation of arteries and veins

Decreased venous return and cardiac output

—induced by sepsis, manifested by continued hypotension in spite of adequate fluid resuscitation. Accompanied by perfusion abnormalities. Mortality rate approaches 60%!!

– progressive physiologic dysfunction in two or more organ systems after acute threat to systemic homeostasis.

Very important to understand—SIRS, sepsis and MODS are primarily exaggerated immune/inflammatory responses!!! They are caused when protective mechanisms become deranged.

Cellular injury or Gram negative bacteria release substance called endotoxin.

Trigger the Inflammatory/Immune Response.

Cytokines released in response to insult.

Chemicals designed to ―call‖ substances needed to the site of injury

Immune/Inflammatory cells and mediators travel by chemotaxis

Tachycardia

MAP < 70; decreased BP

Pulses becoming increasingly thready

Peripheral edema

Skin warm initially then cool and clammy

Crackles or wheezes on auscultation

ABG’s: PaO2 <60 mmHg, PaCO2 >45mmHg

Decreased compliance

Diffuse infiltrates (ARDS)

Frequent manipulation of FiO2 required

REFRACTORY hypoxia

Oliguria or anuria

Creatinine clearance < 30ml/min

BUN >20mg/dl

Serum creatinine > 2.0 or double the creatinine level on admission

Multiple electrolyte abnormalities

WBC >10000 initially, <5000 later

Decreased H/H

Platelets < 100,000

PT >25% above normal

PTT >25% above normal

Fibrin split products >10mcg/ml

Bilirubin >2.0 mg/dl

Albumin < 2.8 g/dl

Liver enzymes >50% above normal

Hyperglycemia initially; hypoglycemia as process continues

Jaundice

Ileus with NGT ouput >600 cc/24hr

Stress ulcers

GI bleed

Dry heat (flames), moist heat (steam, liquids)

More common in children and elderly

Charring of vascular, bone, muscle, and nervous tissue

Acid

Results in coagulation necrosis and protein precipitation, limiting extent of burn

Base

Results in liquefaction necrosis, allowing deeper spread of chemical resulting in more severe burn

Inhalation of hot air or noxious chemicals

CO

Injury above/below glottis

Major predictor of mortality

Treat quickly

Severity depends on type and duration of current, and amount of voltage

Takes path of least resistance- blood vessels and nerves

Coagulation necrosis

Usually sunburns or radiation treatment

Usually superficial

S&S- HA, chills, N/V

Partial-thickness

Superficial partial

Bright red, moist, blister formation

Deep partial

Pale and waxy, moist or dry

May convert to full thickness as necrosis extends

Full-thickness

Involves all layers, may extend to subc fat, connective tissue, muscle and bone

Appears pale, waxy, yellow, charred, or nonblanching red

No sensation of pain or light touch

Requires skin grafting

LR 4mL/kg per % TBSA

Example: 4mL X 80kg X 40% = 12,800 mL

50% administered in first 8 hrs (6400mL or 800mL/hr)

Other 50% over next 16 hours (400mL/hr)

Initial resuscitation complete in 24 hrs

5% Dextrose after resuscitation

May require rates in excess of calculations

Harvest from client

Only way to get permanent closure

Split thickness and full thickness grafts

Cultured epithelial autografting

Within 3-4 weeks enough skin to cover entire body

Problems with lack of attachment

Temporary medium that promotes healing, and prepares wound for permanent coverage

Homograft (allograft)

Skin harvested from cadavers

Heterograft (xenograft)

Harvested from animal, usually pig

Biobrane

Nylon mesh bonded to silicone

Normal CD4 count, what does it indicate when it is severely low, low, normal

Normal: 800-1200 cells/uL

Immune problems start when cell counts drop below 500 cells/uL

Intermediate chronic: cells from 200-500

Late chronic or AIDS: cells below 200

A craniotomy is a type of brain surgery. It is the most commonly performed surgery for brain tumor removal . It also may be done to remove a blood clot (hematoma), to control hemorrhage from a weak, leaking blood vessel (cerebral aneurysm), to repair arteriovenous malformations (abnormal connections of blood vessels), to drain a brain abscess, to relieve pressure inside the skull, to perform a biopsy, or to inspect the brain.

Read more: Craniotomy - procedure, recovery, blood, removal, pain, complications, adults, time, infection, operation, medication, risk, children, cancer, nausea, Definition, Purpose, Demographics http://www.surgeryencyclopedia.com/Ce-Fi/Craniotomy.html#ixzz1dozT2eFG

Why give solumedrol after craniotomy

Results from bleeding between the dura and the inner surface of the skull

Neurologic emergency

Venous or arterial origin

Occurs from bleeding between the dura mater and arachnoid layer of the meningeal covering of the brain

Most common source is the veins that drain the brain surface into the sagittal sinus

Usually venous in origin

Much slower to develop into a mass large enough to produce symptoms

Develops over weeks or months after a seemingly minor head injury

Peak incidence in sixth and seventh decades of life

Presenting complaint often focal symptoms, not signs of increased ICP

Delay in diagnosis in older adults because symptoms mimic those of vascular disease and dementia

Occurs from bleeding within the parenchyma

Usually occurs within the frontal and temporal lobes

Size and location of hematoma determine patient outcome

Stroke risk factors

Risk Factors Nonmodifiable

Age

Gender

Race

Heredity/family history

Risk Factors Modifiable

Hypertension

Metabolic syndrome

Heart disease

Heavy alcohol consumption

Poor diet

Drug abuse

Sleep apnea

Obesity

Physical inactivity

Smoking

• Aphasia
• Visual deficits (partial or full blindness to the right side)
• Difficulty with writing, reading, speech, comprehension, arithmetic
• Difficulty following directions
• Jargon: incoherent speech
• Perseveration: repeating a word or phrase inappropriately
• Right hemiplegia, or paralysis of the right side of the body
• Memory problems may develop along with shortened retention spans
• Struggle to learn new information as well as conceptualizing

• Short attention span
• Left visual field loss
• Poor judgment
• Disorientation
• Denial that there is anything wrong
• Confusion about time and space concepts
• Poor hand-eye coordination and/or balance
• Movement on the left side of the body is impacted
• Left hemiplegia or paralysis in the left side of the body
• Short term memory loss

Recombinant tissue plasminogen activator (tPA)

Used to reestablish blood flow through a blocked artery to prevent cell death in patients with acute onset of ischemic stroke symptoms

Must be administered within 3 hours of onset of clinical signs of ischemic stroke

Aspirin is used within 48 hours of stroke

Platelet inhibitors and anticoagulants may be used in thrombus and embolus stroke patients after stabilization

Contraindicated for patients with hemorrhagic stroke

Metabolism

Increased appetite, weight loss, heat intolerance

Cardiovascular

HTN, tachycardia, palpitations

GI

Hyperactive BS, increased peristalsis

Neuromuscular

Nervousness, restlessness, insomnia, tremor

Other

Fine hair, smooth/warm skin

Thyroid antibodies

TSH

T4, T3

3

Radioactive iodine uptake test

Thyroid suppression test

Drugs

Antithyroid

Beta-blockers

Radioactive Therapy

Damage or destroy cells

Surgery

Subtotal or total thyroidectomy

Risk for decreased cardiac output

Altered Nutrition

Body Image Disturbance

Insufficient amount of thyroid hormone

Defect in thyroid gland

Post hyperthyroid treatment

Thyroditis (Hashimoto’s)

Iodine deficiency

Myxedema

Common in females 30-60

Hypothyroidism

Manifestations

Metabolism

Cold, sleepy, weakness, fatigue

Cardiovascular

Hypotension, bradycardia

GI

Constipation, anorexia, vomiting

Neuromuscular

Slow movement and thinking

Other

Goiter, dry skin and hair

Hypothyroid crisis

Hyponatremia, hypoglycemia, lactic acidosis

Hypothermia, cardiovascular collapse

Precipitated by trauma, infection, uncontrolled hypothyroidism

Maintain airway, correct imbalances

Same as hyperthyroid with opposite results

TSH- elevated

T4, T3- decreased

RAI- decreased

Medications

Replacement therapy

Surgery

For goiter that interferes with airway/swallowing

Hypothyroidism

Nursing Care

Decreased cardiac output

Constipation

Risk for impaired skin integrity

Activity intolerance

Altered thought process

Risk factor

Exposure to ionizing radiation during childhood

More common in females

Palpable firm nodule in thyroid

TH usually normal

Subtotal or total thyroidectomy

Thyroid replacement

Hyperparathyroidism

Collaborative Care

May be d/t tumor or hyperplasia

Hypercalcemia & hypophosphatemia

"Bones, stones, abdominal groans"

Bone decalcification

Renal calculi

Abdominal pain, constipation

Labs

Electrolytes, Ca, Phos, Mag

Treatmemt

Decrease Ca levels

Increase fluid intake

Diuretics (Lasix)

Meds to inhibit bone reabsorption (Fosamax)

Removal of gland

Damage or removal of parathyroid glands

Hypocalcemia & hyperphosphatemia

Numbness, tingling around mouth, tetany

Need long term calcium supplements, Vit D

Excessive production of cortisol

Primary

Benign or malignant adrenal tumor

Secondary

Increased release of ACTH

Iatrogenic

Long term glucocorticoid therapy

Central obesity, buffalo hump, rounded face

Hyperglycemia

Sodium retention

Hypokalemia

Thin, bruising skin

Altered immunity, risk for infection 

Depression

Changes in secondary sex characteristics

Cushing's Lab & Diagnostics, Treatment,

Nursing Care

Plasma cortisol and ACTH levels

24-hour urine

Electrolytes

ACTH suppression test

Medications

Suppress activity of adrenal cortex

Inhibit cortisol synthesis

Surgery

Adrenalectomy

hypophysectomy

Fluid volume excess

Risk for injury/infection

Body image disturbance

Deficiency of cortisol, aldosterone, adrenal androgens

Autoimmune destruction most common cause

Abrupt withdrawal from steroids

Manifestations

Hyponatremia, hyperkalemia, hypoglycemia

Hypotension, syncope

Dizziness, confusion

N/V/D, weakness

Hyperpigmentation of skin

Addison’s Disease

Lab & Diagnostics

Treatment

Nursing Care

Serum cortisol levels

Blood glucose

Electrolytes, CBC

Plasma ACTH

Replacement of corticosteroids

May result in Cushing-like syndrome

Increase dietary sodium

Fluid volume deficit

Knowledge deficit

Tumor of adrenal medulla

Overproduction of catecholamines

Paroxysmal severe hypertension with tachycardia

Adrenalectomy

Causes

Tumor of the adrenal cortex

Chronic kidney disease

Manifestations

HTN, HA, muscle weakness, dysrhythmias

Adrenalectomy, aldactone

Disorders of Anterior Pituitary

gigantism and acromegaly

Gigantism

Hypersecretion of GH prior to puberty

Results in excessively tall stature

Acromegaly

Hypersecretion of GH after puberty

Enlargement of face, hands, feet

High levels of ADH, suppression of aldosterone

Hyponatremia and water intoxication

Neuro symptoms

Decreased LOC, confusion, seizures

Treatment

Restrict fluids, treat underlying cause

Growth Hormone

Prolactin

Thyroid-stimulating hormone (TSH)

Adrenocoricotropic hormone (ACTH)

Gonadotropin hormone

Follicle-stimulating hormone (FSH)

Luteinizing hormone (LH)

Antidiuretic hormone (ADH)

Vasopressin

Oxytocin

Thyroid hormone

T4

T3

Calcitonin

Parathyroid hormone

Catecholamines

Epinephrine

Norepinephrine

Mineralocorticoids

Aldosterone

Glucocorticoids

Cortisol & Cortisone

Glucagon

Insulin

Somatostatin

Pancreatic polypeptide

Androgens

Estrogens

Progesterone

Hormones regulate tissue responses

Feedback mechanisms

Negative

Sensors detect changes in hormone level and respond

Positive

Increased level of one hormone causes another gland to release a hormone

Medical history

Family history

Changes in size or function of organs, skin, hair

Changes in thirst, appetite, weight, energy, sleep

Medications

Change in reproductive functioning

Inspection of skin, hair, nails, facial appearance

Palpate thyroid

Motor function

Sensory function

Musculoskeletal structure

Assess for tetany

Normal Older Adult Variations

Endocrine

Hyperpigmentation of forearms and hands

Decreased hair growth

Nails thick, brittle, yellow

Decreased sensation of touch

Decreased DTR

Autoimmune reaction (Grave’s disease)

Excess secretion of TSH from pituitary

Neoplasms

Thyroiditis

Excessive intake of thyroid meds

Extreme state of hyperthyroidism

Infection, trauma, manipulation of thyroid during surgery can precipitate

Excessive metabolic symptoms

Temp elevation to 102-106

HTN, tachycardia, psychosis, delirium, seizure

Benign, results from either HBV or HCV infections

Low serum transferase levels

Usually does not progress to cirrhosis

Malaise, mild fatigue, hepatomegaly

Diagnosed by liver biopsy

No specific treatment

Life threatening

Progresses to cirrhosis with liver failure

Fatigue is common

Results from hepatotoxic drug administration, HBV or HCV

Liver biopsy plus other dx and lab tests

Hepatitis

Lab & Diagnostic Tests

Anti-HAV

IgM anti-HAV

HBsAG: hepatits B surface antigen

HBeAG

Anti-HBs

Anti-HBe

Anti-HBc-IgM

ADAg

Alkaline phosphatase (ALP)

Gamma-glutamyl transferase (GGT)

Alanine aminotransferase (ALT)

Aspartate aminotransferase (AST)

LDH5

Conjugated & unconjugated bilirubin levels

Prothrombin time

Pre-biopsy preparation

Review the procedure w/ pt

Pt should be NPO for 4-6 hrs before biopsy

Have pt void before biopsy

Record baseline vital signs

Review chart for H&H, platelet count, bleeding & clotting times

Post-procedure

Right after procedure, apply direct pressure

Instruct pt to lie on the right side to keep pressure on the site for two hours

Strict bedrest for at least 6 hours

Monitor vital signs frequently for 4-6 hrs

Notify physician if BP differs markedly from baseline or if pt in severe pain

Keep pt. NPO for two hours. Then resume previous diet

Instruct pt. Not to cough hard or strain for 2-4 hr & avoid lifting or strenuous activities for 1 week

Bedrest

Clear liquids initially then encourage a high calorie, high protein, high carb, low fat diet

Pruritus-frequent skin cleaning

Vitamin supplements (B-complex, K)

Avoid alcohol and drugs detoxified by liver

Emotional support

Home Care Teaching

During acute phase

No sharing of eating utensils, bath towels

Avoid sexual and close personal contact

Avoid hepatotoxic substances

Diffuse inflammation and fibrosis

Drastic structural changes

Significant loss of function

Complications: Portal hypertension, bleeding, ascites, hepatic encephalopathy, esophageal varices, bacterial peritonitis

Portal hypertension

Elevated B/P within portal vein

Blood rerouted to other veins with normally lower B/P (collateral circulation)

Veins affected become engorged & congested

Esophagus

Rectum

Abdomen

Splenomegly

Ascites

r/t increased hydrostatic pressure in vessel lumen

Hypoalbuminemia

Hyperaldosteronism

Esophageal varices

Hepatic encephalopathy

ETOH causes fatty infiltration

Inflammatory cells cause necrosis, fibrosis and destruction

Liver shrinks and becomes nodular

Clinical symptoms: anorexia, malaise,weight loss, low-grade fever, jaundice, ascites, hemorrhage,encephalopathy

Cirrhosis

Labs and Diagnostic Tests

Serum electrolytes

CBC w/ platelets

Bilirubin measurements

Total protein, serum albumin, and ammonia levels

Coagulation studies

Serum glucose values

Liver enzyme studies

Diagnostics

Ultrasound

Liver biopsy

Esophagoscopy

Cirrhosis

pharmacology/surgical procedures

Pharmacology

Diuretics: Spironolactone (Aldactone), furosemide (Lasix)

Laxatives: Lactulose

Vitamin K

Antacids

Avoid meds metabolized by the liver

Surgical Procedures

Sclerotherapy per endoscopic procedure

Paracentesis for severe ascites

Peritoneovenous shunt: LeVeen shunt

Tranjugular intrahepatic portosytemic shunt (TIPS)

Liver transplant

Release of pancreatic enzymes into pancreatic tissue leading to hemorrhage and necrosis

10% mortality rate

Acute or Chronic

Autodigestion of the pancreas

Obstruction by gallstone

Obstruction of bile ducts

Back up of duodenal contents into pancreatic duct

Excess HCL causing sphincter spasm

Acute Pancreatitis

Assessment Findings

Sudden severe pain in middle upper abdominal region that radiates to back

N/V, fever

Abdominal distension and tenderness

Diminished bowel sounds

Shallow, rapid breathing

Tachycardia, hypotension

Restlessness, confusion

Jaundice

Discoloration of abdomen and flanks

Elevated serum amylase and lipase levels

Elevated WBC and serum bilirubin level

Transient elevation in blood and urine glucose levels

AST/ALT may be elevated

In severe cases, serum calcium levels may drop

Abnormal ultrasound & CT of pancreas

Local

Pseudocyst

Abscess

Fistulas

Systemic

Diabetes

Hemorrhage, DIC

Hypovolemic shock

Sepsis

Renal failure

ARDS

Acute pancreatitis

Collaborative Care

Relief of pain

Meperidine

Prevention or alleviation of shock

Albumin

Reduction of pancreatic secretions

NPO w/ NG tube to suction

Cimetidine (Tagamet) or ranitidine (Zantac) IV

Control of fluid and electrolyte imbalance

Lactated Ringer’s Solution

Prevention or treatment of infection

Peritoneal lavage

Antibiotics

Removal of precipitating cause, if possible

Surgery: Cholescystectomy to remove gallstones

Surgical resection of all or part of pancreas to remove necrotic tissue

For pseudocyst or abscess, percutaneous insertion of tubes placed for external drainage

Monitor vital signs

Observe fluid & electrolyte imbalances

Assess respiratory function

Observe for symptoms of tetany

Measures to relieve pain

Maintain hydration/nutrition

Observe for fever & other signs of infection

Progressive, destructive disease of pancreas

Characterized by remissions & recurrences

Inflammation & fibrosis contribute to pancreatic insufficiency & diminished function

Chronic Pancreatitis

Two major types:

Chronic obstructive pancreatitis

Associated with biliary disease

Chronic calcifying pancreatitis

Also called alcohol-induced pancreatitis

Chronic Pancreatitis

Assessment Findings

Upper abdominal pain radiating to the back

N/V with weight loss

Flatulence

Constipation

Steatorrhea

Manifestations of DM

Elevated serum & urinary amylase levels

Elevated serum bilirubin w/ jaundice

Chronic Pancreatitis

Collaborative Care/Nursing Care 

Prevention of further attacks

Relief of pain

Control of pancreatic exocrine & endocrine insufficiency

Diet

Pancreatic enzyme replacement

Control of diabetes

Surgery

Nursing Care

After pancreatitis

Prevention of further attacks

Avoid alcohol, narcotics

Reporting symptoms

Pain, N/V, abdominal distention, steatorrhea, polyuria, polydipsia, polyphagia, weight loss, fever

Low-fat,low protein, high carbohydrate bland diet

Several small meals, vitamin supplements

Continuing medications

Pancreatic enzymes, bile salts, oral hypoglycemic agents or insulin

Need for continued medical follow up

Seek medical care when ill

 glycoprotein produced only in the presence of BPH or Prostate cancer

PSA (prostate specific antigen)

Men with BPH have elevated PSA

Bleeding, clot retention, inability to void, and UTI’s

Very low risk for erectile dysfunction

Decreases osteoporosis risk, lowers colorectal cancer risk (estrogen/progestin)

Increased risk breast CA, stroke, heart disease, DVT, PE (combo)

Increased risk for stroke, DVT, PE (estrogen only)