abc 2011-2012 metabolic alterations
Post on 03-Apr-2018
216 Views
Preview:
TRANSCRIPT
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
1/163
METABOLIC
ALTERATIONS
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
2/163
Clinical Assessment
History
Physical examination
Labs
Diagnostics
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
3/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
4/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
5/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
6/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
7/163
RUQ LUQ
RLQ LLQ
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
8/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
9/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
10/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
11/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
12/163
Test Evaluates Comments
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
13/163
Test Evaluates Comments
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
14/163
Test Evaluates Comments
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
15/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
16/163
E. hystolitica
trophpzoites
G. lamblia
trophzoites
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
17/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
18/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
19/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
20/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
21/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
22/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
23/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
24/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
25/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
26/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
27/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
28/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
29/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
30/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
31/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
32/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
33/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
34/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
35/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
36/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
37/163
Assessment and Diagnostic
Procedures Give the signs and symptoms of dehydration
Why do patients with hyperglycemia become dehydrated?
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
38/163
Assessment and Diagnostic
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
39/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
40/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
41/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
42/163
Pancreas
Diabetes mellitus
Complications: diabetic ketoacidosis, nonketotic
hyperosmolar coma, hypoglycemia, diabetic foot, vascular
diseases
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
43/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
44/163
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 -
7/28/2019 ABC 2011-2012 Metabolic Alterations
45/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
46/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
47/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
48/163
Assessment and Diagnosis
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
49/163
Medical Management
Reverse hydration
Replace insulin
Reverse ketoacidosis
Replenish electrolytes
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
50/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
51/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
52/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
53/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
54/163
Reverse Ketoacidosis
Insulin replacement
Adequate hydration
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
55/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
56/163
Nursing Management
Administering prescribed fluids, insulin, and electrolytes
Monitoring response to therapy
Maintaining surveillance for complications
Providing patient education
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
57/163
Complications
Fluid volume overload
Hypoglycemia
Hypokalemia
Hyperkalemia
Hyponatremia
Risk for cerebral edema
Risk for infection
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
58/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
59/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
60/163
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 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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
61/163
Assessment and Diagnosis
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
62/163
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)
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
63/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
64/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
65/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
66/163
Nursing Management
Administer fluids, insulin, and electrolytes
Monitoring response to therapy
Maintaining surveillance for complications
1. Hypoglycemia
2. Hypokalemia
3. Hyperkalemia
4. Infection
5. CVS, pulmonary, or kidney disease Providing patient education
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
67/163
Acute Pancreatitis
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
68/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
69/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
70/163
Ransons Criteria for Estimating the
Severity of Acute Pancreatitis During initial 48 hours of hospitalization
Fall in hematocrit >10% with hydration or hematocrit
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
71/163
Ransons Criteria for Estimating the
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
72/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
73/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
74/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
75/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
76/163
Assessment and Diagnosis
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
77/163
Assessment and Diagnosis
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
Assessment and Diagnosis
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
78/163
Assessment and Diagnosis
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)
Assessment and Diagnosis
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
79/163
Assessment and Diagnosis
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
80/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
81/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
82/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
83/163
Medical Management
Local complications
1. Infected pancreatic necrosis and pancreatic pseudocyst
2. Management is surgical debridement, drainage of the
pseudocyst contents, antibiotics
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
84/163
Nursing Management
Providing pain relief and emotional support opioids andrelaxation techniques
Maintaining surveillance for complications
Educating the patient and the family
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
85/163
Fulminant Hepatic Failure
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
86/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
87/163
Common Laboratory Studies of Liver Function
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
88/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
89/163
Test Normal values Interpretation
Total bilirubin
Urine bilirubin
Urine urobilinogen
Albumin
Globulin
Total proteins
A/G ratio
Transferrin
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
90/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
91/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
92/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
93/163
Assessment and Diagnosis
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
94/163
Assessment and Diagnosis
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
95/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
96/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
97/163
Nursing Management
Protecting the patient from injury
Maintaining surveillance for complications
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
98/163
Acute Gastrointestinal
Hemorrhage
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
99/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
100/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
101/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
102/163
Assessment and Diagnosis
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
103/163
Class Blood loss (%) Clinical S/Sx
1
2
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
104/163
A t d Di i
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
105/163
Assessment and Diagnosis
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
106/163
Assessment and Diagnosis
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
107/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
108/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
109/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
110/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
111/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
112/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
113/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
114/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
115/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
116/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
117/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
118/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
119/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
120/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
121/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
122/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
123/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
124/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
125/163
Medical Management
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
126/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
127/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
128/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
129/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
130/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
131/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
132/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
133/163
Hyperthyroidism Thyroid Storm
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
134/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
135/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
136/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
137/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
138/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
139/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
140/163
Assessment and Diagnostic Findings
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
141/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
142/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
143/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
144/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
145/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
146/163
Nursing Implications
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
147/163
g p
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
148/163
y
Thyrotoxicosis Thyrotoxic crisis
Severe hyperthyroidsm, usually abrupt in onset
If left untreated, almost always fatal
First what causes hyperthyroidism?
?
TRH
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
149/163
Thyroid gland
?
Anterior pituitarygland
T3 and T4
Iodine from food
and other sources
LiverTarget organs
Negativefeedback
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
150/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
151/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
152/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
153/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
154/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
155/163
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
156/163
Thyroid Storm
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
157/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
158/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
159/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
160/163
Management
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
161/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
162/163
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
-
7/28/2019 ABC 2011-2012 Metabolic Alterations
163/163
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
top related