ABC 2011-2012 Metabolic Alterations

7/28/2019 ABC 2011-2012 Metabolic Alterations

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METABOLIC

ALTERATIONS


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Clinical Assessment

History

Physical examination

Labs

Diagnostics


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Physical Examination

Inspection

1. Oral cavity

2. Skin over the abdomen

3. Shape of the abdomen

Auscultation1. Bowel sounds

2. Presence of bruits

Percussion

1. Assessment of the deep organs

Palpation

1. Light palpation approximately 1 cm deep

2. Deep palpation depth of 4 to 5 cm


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Physical Examination

Anatomic correlates of four abdominal quadrants:

1. RUQ: liver and gallbladder, pylorus, duodenum, head of the

pancreas, right adrenal gland, portion of right kidney, hepatic

flexure of colon, portions of ascending and transverse colon

2. RLQ: lower pole of the right kidney, cecum and appendix,portion of ascending colon, bladder (if distended), ovary and

salpinx, uterus (if enlarged), right spermatic cord, right ureter

3. LUQ: left lobe of the liver, spleen, stomach, body of the

pancreas, left adrenal gland, portion of the left kidney, splenicflexure of colon, portions of transverse and descending colon

4. LLQ: lower pole of left kidney, sigmoid colon, portion of the

descending colon, bladder (if distended), ovary and salpinx,

uterus (if enlarged), left spermatic cord, left ureter


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Abnormal Abdominal SoundsSound Description Causes

Borborygmi

Bowel sounds

Decreased bowel sounds

Absence of bowel sounds

Hyperactive bowelsounds; loud and

prolonged

High-pitched, tinkling

sounds

Hypoactive bowel sounds;

infrequent abnormally

faint

Confirmed only after

consultation of all four

quadrants and continuous

auscultation for 5

minnutes

HungerGastroenteritis

Early intestinal obstruction

Intestinal air/fluid under

pressure; characteristic of

early intestinal obstruction

Possible peritonitis or

ileus

Temporary loss ofintestinal motility, as with

complete ileus


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Abnormal Abdominal SoundsSound Description Causes

Friction rubs

Bruits

Venous return

High-pitched sounds overthe liver/spleen,

synchronous with

respiration

Audible swishing soundsover aorta, iliac, renal,

and femoral arteries

Low-pitched, continuous

sound

Pathologic conditions(e.g., tumors, infection)

that cause inflammation of

organs peritoneal

covering

Abnormality of blood flow(requires additional

evaluation to determine

specific disorder)

Increased collateral

circulation between portaland systemic venous

systems


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RUQ LUQ

RLQ LLQ


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Selected Laboratory Studies of GI

FunctionTest Normal findings Clinical significance of

abnormal findings

Stool studies Resident microorganisms:

clostridia, enterococci,

Pseudomonas, a few

yeast cells

Fat: 2-6 g/24 hr

Salmonella typhi

Shigella

Vibrio cholerae

YersiniaE. Coli

S. Aureus

C. Botulinum

C. Perfringens

Aeromonas

Steatorrhea (increased

values) from intestinal

malabsorption or

pancreatic insufficiency


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Selected Laboratory Studies of GI

FunctionTest Normal findings Clinical significance ofabnormal findings

Stool studies

Culture and sensitivity of

duodenal contents

Pus: none

Occult blood: none

(orthotolidine,

guiaiac test)

Ova and parasites

No pathogens

Large amounts associated with

chronic ulcerative colitis,

abscesses, anal-rectal fistula

Positive tests associated with

bleeding

E. hystolitica, G. lamblia, worms

Salmonella typhi, etc


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Abdominal Diagnostic ProceduresTest Evaluates Comments

Barium enema (also

called lower GI series)

Visualizes movement,

position and filling of

various segments of

colon after instillation

Diagnoses colorectal

lesions, diverticulitis,

inflammatory boweldisease, strictures,

fistulas

Evaluates colon size,

length, patency

Low-fiber diet for 1-3 days before

study

Bowel preparation with bowel

irrigation and cathartics

NPO for 8-12 hours before study

Cathartics must be given after

study

Contraindicated if bowel

perforation or obstruction exists


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Test Evaluates Comments

Barium swallow (also

known as upper GI

series and small

bowel follow-

through)

Visualizes position,

shape, and activity of

esophagus, stomach,

duodenum, and

jejunum

Diagnoses esophageal

lesions/varices or

motility disorders, hiatal

hernia, gastriculcers/tumors, small

bowel obstruction,

small bowel lesions,

Crohns disease

Evaluates gastric and

small bowel motility

Bowel preparation with irrigation

and cathartics

NPO for 8-12 hours before

study

Cathartics must be given after

studyContraindicated if bowel

perforation or obstruction exists


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Angiography (celiac

or mesenteric)

Evaluates portal

vasculature

Diagnoses source of

bleeding

Evaluates cirrhosis,

portal hypertension,

vascular damage

resulting from trauma,

intestinal ischemia,tumors

May be used to treat GI

bleeding

Bowel preparation as prescribed

NPO for 8h before study

Sedative usually prescribed

before procedure

If contrast media is used, check

for history of allergy to iodine

before study and monitor, ensure

hydration

Always monitor for signs of

bleeding during after studyCheck for the neurovascular

status of the affected extremity


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CT scan

Endoscopy

* Esophagogastrocospy

(EGD)*Colonoscopy

Diagnoses tumors,

pancreatic cancer or

cysts, pancreatitis,

biliary disorders,

obstructive versus

nonobstructive

jaundice, cirrhosis,

liver metastases,

ascites, lymph nodemetastases,

aneurysm

Directly visualizes

mucosa of areas in

GIT

No special preparation required

Sedation may be prescribed,

specially for colonoscopy

Bowel preparation with gastricirrigation and cathartics required

before lower GI endoscopy

NPO 4-8 hours before study


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Liver biopsy

Ultrasound

Obtains tissue for specimen

evaluation

Diagnoses liver disease or

malignancy

Evaluates pancreas, biliary

ducts, GB, liver

Identifies tumor, abdominal

abscesses, hepatocellulardisease, splenomegaly,

pancreatic or splenic cysts

Differentiates obstructive form

nonobstructive jaundise

Open biopsy done in surgery

Closed biopsy may be done at

bedside; contraindicated if

platelets


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E. hystolitica

trophpzoites

G. lamblia

trophzoites


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Assessment and Diagnostic

Procedures Pancreas

1. History (1) current health status, (2) history of presentillness, (3) past history of and general endocrine status, and(4) family history

2.Physical assessment hyperglycemiaa. Inspection flushed skin, polyuria, polydipsia, vomiting, andevidence of dehydration; progressive deterioration of level ofconsciousness from alert to lethargic or comatose; breathingbecomes deep and rapid (Kussmaul respirations), andbreath may have fruity odor

b. Auscultation hypoactive bowel sounds

c. Palpation abdominal tenderness

d. Percussion diminished deep tendon reflexes


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Procedures Give the signs and symptoms of dehydration

Why do patients with hyperglycemia become dehydrated?


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Procedures Pancreas Laboratory studiesa. Plasma glucose short term

b. Glycated hemoglobin long term

c. Fasting plasma glucose (FPG) normal is 70 to 110 mg/dL

d. Urine glucose not recommended for diabetic patientsbecause of too much variation in the renal threshold forglucose

e. Glycated hemoglobin useful for daily management ofdiabetes (Hbaic), normal is 4% to 6%

f. Blood ketones normal is 2 to 4 mg/dL

g. Urine ketones normally, only minute traces can be foundh. Serum amylase normal is 40 to 180 U/l


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Plasma Blood Glucose Levels

Patient Status mg/dl Mmol/L

Hypoglycemia

Normal FPG

Impaired FPG

FPG diagnostic of DM

Non-FPG diagnostic of

DM

Below 70

70 to 110

110 126

Above 126

Above 200

Below 3.9

3.9 to 6.1

6.1 to 7.0

Above 7.0

Above 11.1


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Common Laboratory Studies of Pancreatic Function

Test Normal value Clinical significance

Serum amylase

Serum lipase

Urine amylase

Secretin test

Stool fat

60-180 Somogyi units/ml

1.5 Somogyi units/ml

35-260 Somogyi units/ml

Volume 1.8 ml.kg/h

HCO3 concentration: >80

mEq/L

HCO3 output: >10

meq/L/30 sec

2-5 g/24 hr

Elevated levels with pancreatic

inflammation

Elevated levels with pancreatic

inflammation

May be elevated with other

conditions

Elevated levels with pancreaticinflammation

Decreased volume with

pancreatic disease (secretin

stimulates pancreatic

secretion)

Measures fatty acids:

decreased pancreatic lipase

increases stool fat


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Pancreas

Diabetes mellitus

Complications: diabetic ketoacidosis, nonketotic

hyperosmolar coma, hypoglycemia, diabetic foot, vascular

diseases


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Diabetic Ketoacidosis

DKA

A life-threatening complication of diabetes mellitus

Type I DM patients are typically affected

Some elderly with type II DM can also develop DKA Diagnostic criteria:

1. Blood glucose level greater than 250 mg/dL

2. Arterial pH below 7.3

3. Serum bicarbonate level below 18 mEq/L4. Moderate ketonemia or ketonuria

Lack of insulin


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Lack of insulin

liverto turn fat into ketone bodies

decreases the blood'spH

acidosis

Diabetic ketoacidosis

Dehydration, deep rapid breathing, deteriorating levels of consciousness

I li d fi i
http://en.wikipedia.org/wiki/Liverhttp://en.wikipedia.org/wiki/Ketone_bodieshttp://en.wikipedia.org/wiki/PHhttp://en.wikipedia.org/wiki/PHhttp://en.wikipedia.org/wiki/Ketone_bodieshttp://en.wikipedia.org/wiki/Ketone_bodieshttp://en.wikipedia.org/wiki/Ketone_bodieshttp://en.wikipedia.org/wiki/Liver


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Insulin deficiency

Increase glucagon

Gluconeogenesis

Increase fat

metabolism

Ketogenesis

Ketonemia

Decreased

serum pH

Decrease use of glucose by

cells

Decrease glucagon

Hyperglycemia Gluconeogenesis

Glycosuria

Osmotic diuresis

Polyuria

Increase protein

metabolism

Decrease protein

synthesis

Increase amino

acids to liver

Increase blood

urea

Decreas

e Na

AcidosisNausea and vomiting

Decrease Na,

K, P, HCO3Electrolyte

imbalance

Dehydration


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Acidosis Dehydration Increase blood

urea

Kussmaulbreathing

and

excretion of

acetone by

lungs

Hyperosmolality Increase ureanitrogen

Hemoconcentration

Hypotension Tissue hypoxia

Decrease renal

blood flow

Increase lactic

acid

Shock

Coma

Death

Negative nitrogen

balance


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Assessment and Diagnosis

Decreased cardiac output related to alterations in preload

Deficient fluid volume related to absolute loss

Anxiety related to threat to biologic, psychologic, and/or

social integrity

Disturbed body image related to functional dependence

on life-sustaining technology

Ineffective coping related to situational crisis and personal

vulnerability

Powerlessness related to lack of control over current

situation and/or disease progression


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Malaise, headache, polyuria, polydipsia, and polyphagia

Nausea, vomiting, extreme fatigue, dehydration, and

weight loss

CNS depression, with changes in the level of

consciousness

Coma

Labs: urine ketones and hyperglycemia on bedside

fingerstick, metabolic acidosis, low CO2, elevated anion

gap, low serum Na, normal to low serum K


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Medical Management

Reverse hydration

Replace insulin

Reverse ketoacidosis

Replenish electrolytes


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Reverse Hydration

Isotonic saline (0.9% NaCl) IV to replenish the vascular

deficit and to reverse hypotension

1 L of normal saline, infused immediately for severely

dehydrated patients

0.9% NaCl if serum Na is low

0.45% NaCl (hypotonic) if serum osmolality is high and

serum Na is elevated, following initial normal saline

infusion

The replacement infusion typically includes 20 to 30 mEq

of K per liter to restore the intracellular K debt, provided

kidney function is normal


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Reverse Hydration

Fluid replacement should correct intravascular volumedeficits within 24 hours

Careful attention to avoid fluid overload for patientswithout normally functioning kidneys or with CVS disease

Once serum glucose level has decreased to 200 mg/dl,the infusing solution is changed to 50/50 mix of 5%dextrose (D5W) and hypotonic salineto replenishdepleted cellular glucose as the circulating serum glucoselevel falls and to prevent unexpected hypoglycemia when

the insulin drip is continued, before the patient can take insufficient carbohydrate from an oral diet


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Replace Insulin

Moderate to severe DKA initial IV bolus of regular insulin at

0.1 units for each kg (units/kg) of BW

Subsequent infusions of regular insulin at 0.1 units/kg/hr,

simultaneously with IV fluids

Compute: how much insulin should be given per hour to apatient who is 70 kg in weight?

1. For this client, if the plasma glucose level does not fall by 50

to 70 mg/dl in the first hour of treatment, recheck the glucose

measurement and reevaluate the hydration status

2. The insulin infusion should be adjusted until a steady glucose

decline between 50 to 70 mg/dl is achieved


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Replace Insulin

Initially blood glucose tests are performed hourly;

frequency decreases to every 2 to 4 hours as the patients

blood glucose level stabilizes to normal

Once the blood glucose level has decreased to 200 mg/dl,

acidosis is corrected, and rehydration is achieved, it willbe possible to decrease the insulin infusion rate to 0.05 to

0.1 unit per kg body weight, hourly

Important: verify that the serum K is not below 3.3 mEq/L

and to replace serum K if necessary before administeringthe initial insulin bolus


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Reverse Ketoacidosis

Insulin replacement

Adequate hydration


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Replenish Electrolytes

Potassium chloride (KCl) administration begins as soon

as the serum K falls below normal

Phosphate replacement if it falls below 1 mg/dl


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Nursing Management

Administering prescribed fluids, insulin, and electrolytes

Monitoring response to therapy

Maintaining surveillance for complications

Providing patient education


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Complications

Fluid volume overload

Hypoglycemia

Hypokalemia

Hyperkalemia

Hyponatremia

Risk for cerebral edema

Risk for infection


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NKHHS

Nonketotic Hyperglycemic Hyperosmolar Syndrome

Potentially lethal complication of type 2 DM

Hallmarks: extremely high plasma glucose,

hyperosmolality, diuresis and absent or mild ketosis

Diagnostic criteria:

1. Blood glucose level above 600 mg/dl

2. Arterial pH above 7.3

3. Bicarbonate level greater than 15 mEq/L4. Minimal ketonemia and ketonuria

High blood glucose levels


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High blood glucose levels

Water is osmotically drawn out of the cells

into the blood

Glucose is dumped by the kidneys into the urine

Concomitant loss of water increasing blood osmolality

Dehydration and electrolyte imbalance

Malaise, polyuria, polydipsia,

weight loss

Progressive dehydration: mental

confusion, convulsions

Coma

Urine shows

minimal ketones

Minimal or

absent

ketonemia


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Decreased cardiac output related to alterations in preload Deficient fluid volume related to absolute loss

Anxiety related to threat to biologic, psychologic, and/or socialintegrity

Deficient knowledge: discharge regimen related to previouslack of exposure to information

Clinical manifestations:

1. initially, nonspecific

2. Malaise, blurring of vision, polyuria, ploydipsia, weight loss,

and advancing weakness3. Progressive dehydration follows and leads to mental

confusion, convulsions, and eventually coma


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PE: signs of severe dehydration including decreased CVP,

with increases in HR and RR (Kussmaul air hunger is not

present), decreasing LOC

Labs:

1. Plasma glucose above 600 mg/dl

2. Serum osmolality generally above 320 mOsm/L

3. pH is above 7.3

4. Serum bicarbonate greater than 15 mEq/L

5. Absent or mild ketonuria

6. Additional labs: electrolytes


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Medical Management

Rapid rehydration

1. Physiologic saline solution (0.9%) infused at 1L/hr,

specially for a patient in hypovolemic shock

2. Monitor serum sodium to determine when to change from

isotonic to (0.9%) to hypotonic (0.45%) saline3. Sodium input should not exceed the amount required to

replace the losses

4. When serum glucose falls to the 200 to 250 mg/dl range

change the hydration solution to 5% dextrose-0.45% saline

solution (D5W-045%NaCL) at 150 to 250 ml/hr (to prevent

hypoglycemia)


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Medical Management

Insulin administration1. Initially administer an IV bolus of regular insulin (0.1 unit

per kg body weight)

2. Then continuous insulin drip

3. Regular insulin infusing at an initial rate calculated as0.1 unit/kg/hr (7 units/hr for a person weighing 70 kg)

4. When serum glucose reaches 300 mg/dl, the regularinsulin infusion is reduced to 0.5 to 1 unit/kg/hr tomaintain the serum glucose level between 250 to 300mg/dl until serum osmolality is below 315 mOsm/L andthe person is mentally alert


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Medical Management

Insulin resistance

1. Patients with HHS have underlying type 2 DM, and

many will have metabolic syndrome and exhibit signs of

insulin resistance

2. Patients may require high doses of insulin

3. Hourly serial monitoring of blood glucose to avoid

hypoglycemia

4. Oral hypoglycemic agents are then used once the

patient is over the hyperglycemic crisis


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Medical Management

Electrolyte replacement

1. Increasing the circulating levels of insulin with

therapeutic doses of IV insulin will promote the rapid

return of potassium and phosphorus into the cell

2. Serial monitoring of serum electrolyte levels to providethe basis for electrolyte replacement

3. Potassium is typically added to the IV infusion

4. If the serum K level is below 3.3 mEq/L give K first

before giving insulin


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Nursing Management

Administer fluids, insulin, and electrolytes

Monitoring response to therapy


1. Hypoglycemia

2. Hypokalemia

3. Hyperkalemia

4. Infection

5. CVS, pulmonary, or kidney disease Providing patient education


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Acute Pancreatitis


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Acute Pancreatitis

An inflammation of the pancreas that produces exocrinedysfunction that may also involve surrounding tissues

and/or remote organ systems

Clinical course: mild, self-limiting, to systemic process

characterized by organ failure, sepsis, and death Two most common causes of acute pancreatitis are

gallstones and alcoholism

Less common causes: surgical trauma, hypercalcemia,

various toxins, ischemia, infections, and use of certaindrugs

Idiopathic causes: 10 to 20% of cases

R C it i f E ti ti th


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Ransons Criteria for Estimating the

Severity of Acute PancreatitisAt admission

Age >55 years

Hypotension

Abnormal pulmonary findings

Abdominal massHemorrhagic or discolored peritoneal fluid

Increased serum LDH levels (>350 units/L)

AST >250 units/L

Leukocytes (>16,000/mm3)Hyperglycemia (>200 mg/dl; no diabetic history)

Neurologic deficit (confusion, localizing signs)

R C it i f E ti ti th


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Severity of Acute Pancreatitis During initial 48 hours of hospitalization

Fall in hematocrit >10% with hydration or hematocrit


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Severity of Acute Pancreatitis If the patient has up to two factors present, predicted

mortality is 1%

With three to four factors, 15% to 20% mortality

With five to six factors, 40% mortality

With seven or eight factors, 100% predicted mortality

Obstruction or damage to the

pancreatic duct systemKallikrein and chymotrypsin results in


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Premature activation of

digestive enzymes (Trypsin)

pancreatic duct system,

alterations in the secretory

processes of the acinar cells,

infection, ischemia, and/or

other unknown factors

Proteolytic enzymes

(kallikrein, chymotrypsin,

elastase, phospholipase A,and lipase) are triggered

Autodigestion of the pancreas

begins

increase capillary permeability = plasma

leakage = relative hypovolemia

Elastase dissolves elastic fibers of blood

vessels and ducts = hemorrhage

Phospholipase A + bile = phospholipids

of cell membranes causing severe

pancreatic and adipose tissue necrosis

Lipase flows into the damaged

tissue and is absorbed into the

systemic circulation = fat necrosis

of the pancreas and surrounding

tissua


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Pain

Vomiting Nausea

Fever

Abdominal distention

Abdominal guarding

Abdominal tympany Hypoactive/absent bowel sounds

Severe disease:

Peritoneal signs

Ascites

Jaundice

Palpable abdominal mass

Grey Turners sign

Cullen sign

Signs of hypovolemic shock



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Labs: serum amylase (specific for acute

pancreatitis) and lipase, CBC (leukocytosis),

calcium (hypocalcemia), glucose (hyperglycemia),

bilirubin (hyperbilirubinemia), albumin

(hypoalbuminemia)

Diagnostics: abdominal UTZ, MRI, ERCP,abdominal films (flat plate and upright or decubitus),

chest films (PA and lateral)



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Acute pain related to transmission and perception of

percutaneous, visceral, muscular, ischemia

impulses

Deficient fluid volume related to relative loss

Decreased cardiac output related to alterations in

preload

Anxiety related to threat to biologic, psychologic,

and/or social integrity

Deficient knowledge: discharge regimen related to

lack of previous exposure to information


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Medical Management

Fluid management

1. IV crystalloids and colloids

2. Pulmonary catheter to guide ongoing fluid management

3. Monitor electrolytes closely

4. Correct hypokalemia and hypomagnesemia

5. Insulin for hyperglycemia


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Medical Management

Systemic complications1. Hypovolemic shock

2. Acute lung injury

3. Acute renal failure

4. GI hemorrhage5. CVS: hypotension, pericardial effusion, ST-T changes

6. Hematologic: DIC, thrombocytosis, hyperfibrinogenemia

7. CNS: fat emboli, psychosis, encephalopathy

8. Ophthalmic: Purtschers retinopathy sudden blindness

9. Dermatologic: subcutaneous fat necrosis


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Medical Management

Local complications

1. Infected pancreatic necrosis and pancreatic pseudocyst

2. Management is surgical debridement, drainage of the

pseudocyst contents, antibiotics


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Nursing Management

Providing pain relief and emotional support opioids andrelaxation techniques


Educating the patient and the family


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Fulminant Hepatic Failure


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Common Laboratory Studies of Liver Function


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Common Laboratory Studies of Liver Function

Test Normal values Interpretation

Alkaline phosphatase

Aspartate transferase

(AST)

Alanine transferase (ALT)

Lactate dehydrogenase(LDH)

5-Nucelosidase

Indirect bilirubin (B1)

Direct bilirubin (B2)

13-39 units/ml

5-40 units/ml

5-35 units/ml

200-500 units/ml

2-11 units/ml


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Test Normal values Interpretation

Total bilirubin

Urine bilirubin

Urine urobilinogen

Albumin

Globulin

Total proteins

A/G ratio

Transferrin


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Fulminant Hepatic Failure

A life-theatening condition characterized by severe andsudden liver cell dysfunction, coagulopathy, and hepaticencephalopathy

Generally occurs in patients with pre-existing liver disease

Causes:1. Infections

2. Drugs

3. Toxins

4. Hypoperfusion5. Metabolic disorders

6. Surgery


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Liver flaps inability to voluntary sustain a fixed position of theextremities

Asterixis patient extends the arms and dorsiflex the wrists,resulting in downward flapping of the hands

Hepatic encephalopathy (Staging):

I.Euphoria or depression, mild confusion, slurred speech,disordered sleep rhythm, slight asterixis, and normal EEG

II. Lethargy, moderate confusion, marked asterixis and abnormalEEG

III. Marked confusion, incoherent speech, sleeping butarousable, asterixis present and abnormal EEG

IV. Coma, initially responsive to noxious stimuli, laterunresponsive; asterixis absent


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Ineffective breathing pattern related to decreased lungexpansion

Impaired gas exchange related to ventilation/perfusion

mismatching or intrapulmonary shunting

Decreased cardiac output related to alterations in preload

Disturbed body image related to actual change in body

structure, function, or appearance


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Medical Management

Neomycin or lactulose to remove or decrease production ofnitrogenous wastes in the large intestine

Neomycin oral or rectal administration in order to reduce thebacterial flora of the colon to decrease the formation ofammonia

Side effects of neomycin: nephrotoxicity and hearingimpairment

Lactulose (synthetic keto-analog of lactose) split into lacticacid and acetic acid in the intestine, creating an acidicenvironment decreasing bacterial growth; administered orally,via NGT or as retention enema

Lactulose also traps ammonia and has a laxative effect thatpromotes expulsion


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Medical Management

Prevent and watch out for complications:

1. Bleeding phytonadione, FFP, platelet transfusion

2. Increase ICP

3. Metabolic disturbances: hypoglycemia, metabolic

acidosis, hypokalemia, and hyponatremia appropriate

fluids and electrolytes

4. Infection - antibiotics


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Nursing Management

Protecting the patient from injury


Educating patient and family

1. Specific etiology

2. Precipitating factor modification

3. Interventions to reduce further episodes

4. Importance of taking medications

5. Lifestyle changes6. Diet modification

7. Alcohol cessation


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Acute Gastrointestinal

Hemorrhage


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Acute GI Hemorrhage

A medical emergency

Etiology

Upper GI

1. PUD

2. Stress ulcers

3. Esophageal varices

4. Mallory-Weiss tear

5. Neoplasm6. Aortoenteric fistula

7. Angiodysplasia


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Acute GI Hemorrhage

A medical emergency Etiology

Lower GI

1. Diverticulitis

2. Angiodysplasia3. Neoplasm

4. Inflammatory bowel disease

5. Infectious colitis

6. Radiation colitis

7. Ischemia

8. Aortoenteric fistula

9. Hemorrhoids

G


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Acute GI Hemorrhage

Stress UlcersA term used to describe the gastric mucosal abnormalities

often found in the critically patient that develop in

response to severe stress in other organs

Develop rapidly within 24 hoursEsophageal varices

Engorged and distended blood vessels of the esophagus

and proximal stomach that develop as a result of portal

hypertension secondary to hepatic cirrhosis

A d Di i


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Hematemesisbright-red or coffee ground, what is theamount?

Hematochezia massive lower GI bleeding and if rapid

enough, upper GI bleeding

Melena upper GI bleeding

Clinical Classification of Hemorrhage


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Class Blood loss (%) Clinical S/Sx

1

2


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A t d Di i


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Deficient fluid volume related to absolute loss Decreased cardiac output related to alterations in preload

Powerlessness related to health care environment or

illness-related regimen

Deficient knowledge: discharge regimen related to lack ofprevious exposure to information

A t d Di i


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Labs: CBC with platelet count, PT, stool examination Diagnostics: urgent fiberoptic endoscopy stabilize the

patient hemodynamically prior to endoscopy and the area

to be visualized should be cleared of blood


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Medical Management


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Medical Management

Control bleeding PUD1. Thermal injection uses heat to cauterize the bleeding

vessle

2. Hypertonic saline, epinephrine, ethanol and sclerosants

injection to cause vasoconstriction

3. Endoscopic clips

4. Intraarterial infusion of vasopressin into the gastric artery

5. Intraarterial injection of an embolizing agent (Gelfoam

pledgets, stainless steel coils, platinum microcoils, and

polyvinyl alcohol particles) can also be performed during

arteriography to control bleeding once the site has been

identified


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Hyperthyroidism Thyroid Storm


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Assessment and Diagnostic Findings


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Assessment and Diagnostic Findings

Inspection : normally rises with swallowing, (+/-)asymmetry, swelling

Palpation: size, shape, consistency, (+/-) tenderness,

nodules

Auscultation: (+/-) bruit Labs: TSH, serum T3 and T4, TBG, T3 resin uptake test

(indirect measurement of unsaturated TBG; purpose is to

determine the amount of thyroid hormone bound to TBG),

thyroid antibodies, serum thyroglobulin Diagnostics: RAIU, FNAB, thyroid scan, UTZ


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Nursing Implications


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Medical history which includes medications taken,specially those that contain iodine (multivitamins, cough

syrups, amiodarone), salicylates, amphetamines, steroids,

diuretics

Nurses make note of these medications on the request

Thyroid Storm


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y

Thyrotoxicosis Thyrotoxic crisis

Severe hyperthyroidsm, usually abrupt in onset

If left untreated, almost always fatal

First what causes hyperthyroidism?

?

TRH


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Thyroid gland

?

Anterior pituitarygland

T3 and T4

Iodine from food

and other sources

LiverTarget organs

Negativefeedback


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Thyroid Storm


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Clinical manifestations:1. High fever above 38.5C

2. Extreme tachycardia (more than 130 bpm)

3. Exaggerated symptoms of hyperthyroidism with

disturbances of a major system: weight loss, diarhhea,abdominal pain, edema, chest pain, dyspnea,

palpitations, etc

4. Altered neurologic or mental state, which frequently

appears as delirium psychosis, somnolence, or coma

Thyroid Storm


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Clinical manifestations:1. High fever above 38.5C

2. Extreme tachycardia (more than 130 bpm)

3. Exaggerated symptoms of hyperthyroidism with

disturbances of a major system: weight loss, diarhhea,abdominal pain, edema, chest pain, dyspnea,

palpitations, etc

4. Altered neurologic or mental state, which frequently

appears as delirium psychosis, somnolence, or coma

Thyroid Storm


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It is usually precipitated by stress (injury, infection, thyroidand nonthyroid surgery, tooth extraction, insulin reaction,

DKA, pregnancy, digitalis intoxication, abrupt withdrawal

of antithyroid medication, extreme emotional stress, or

vigorous palpation of the thyroid)

Management immediate goals are reduction of body

temperature and heart rate and prevention of vascular

collapse


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Management


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Hypothermia mattress or blanket, ice packs, a coolenvironment, hydrocortisone and acetaminophen

Humidified oxygen to improve tissue oxygenation and to meetthe high metabolic demands

IV fluids containing dextrose to replace the liver glycogen

stores that have been decreased in the hyperthyroid patient PTU or methimazole to impede formation of T3 and T4 and

block conversion of T4 to T3, the more active thyroid hormoneform

Hydrocortisone to treat shock or adrenal insufficiency

Iodine to decrease output of T4 Meds like propanolol for HF and dysrhythmias

Management


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Surgery is now only being used for special conditions:1. Pregnant women who are allergic to antithyroid meds

2. Patients who are unable to take medications

3. Obstructive symptoms

Surgery is done soon after the thyroid function hasreturned to normal (4 to 6 weeks)

Subtotal thyroidectomy

Total thyroidectomy

PTU is given for rapid normalization of the thyroid priorto surgery

Management


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A beta-blocker may be used to decrease the HR andother signs and symptoms of hyperthyroidism

Iodine (Lugols solution or KI) may be prescribed in an

effort to reduce blood loss post-op

Monitor patients receiving iodine medications for signs ofiodine toxicity (swelling of the buccal mucosa, excessive

salivation, coryza, and skin erruptions) immediate

discontinuation

Documents

ABC 2011-2012 Metabolic Alterations