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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
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Assessment
This patient has the typical features of pituitary apoplexy. The lack of fever and the acute onset
make meningitis less likely. SAB needs to be considered as a possibility, but the existence of
prior adenoma make apoplexy more likely. In any event, CT without contrast will help to
differentiate the two.
Further Management Plan/Results
Initial Management
The ICU setting is required, since pituitary apoplexy is considered an endocrinologic
emergency.
In patients with acute visual loss, neurosurgeons sometimes perform an emergency
transsphenoidal resection.
Discussion
Pituitary MRI: confirms existence of pituitary macroadenoma with acute hemorrhage; MRI
findings also show that the tumor was displacing the optic chiasm, explaining the acute
visual field changes.
Cortisol level: low
TSH level: low
FSH and LH: low
Initiate hormone replacement with hydrocortisone and levothyroxine
Start IV fluids to stabilize BP
Initiate neurosurgery consult if surgical intervention needed
471
Pituitary apoplexy is an emergency that causes acute hypopituitarism. It is typically due to
bleeding into or impaired blood supply of the pituitary. It occurs in the presence of a pituitary
adenoma (or another pituitary tumor, <30% of cases).
The most common initial symptom (>90%) is sudden headache, often associated with blurry
vision and worsening visual field defects. This is caused by compression of the nerves around
the optic chiasm. The oculomotor nerve is predominantly affected as it lies closest to the
pituitary. It is also commonly associated with nausea and vomiting. In 25% of cases, the
presence of blood irritates the meninges, which may cause neck stiffness and photophobia.
This initial stage is then followed by hormonal defects. Especially important is adrenal
insufficiency (70% of cases) and is due to a decrease in production of ACTH. The sudden
decrease in cortisol production causes an adrenal crisis (Addisonian crisis). This may cause
hypotension (as noted in our patient) and hypoglycemia. The hypotension and hypoglycemia can
be life-threatening and require immediate intervention.
Hypornatremia may occur and can be profound. It is thought to be due to the low cortisol or
elevated levels of ADH (inappropriate secretion). Several other hormonal deficiencies may
develop in the subacute phase including deficiency in TSH, LH, and FSH. This leads to
hypothyroidism, and in women amenorrhea and infertility.
Diagnosis is confirmed by MRI scan of the pituitary, which may demonstrate hemorrhage or
infarction (due to reduced blood supply). Note: It makes sense to start with CT scan without
contrast in the emergency department, in order to rule out SAB. The hormonal dysregulation is
confirmed by showing low levels of ACTH (and cortisol), TSH and FSH and LH.
Treatment is timely correction of hormone deficiencies and in some cases, surgical
decompression (neurosurgery consult). The decision on whether to neurosurgically decompress
the pituitary gland will depend on the severity of visual loss and visual field defects. Most
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patients will need long-term hormonal supplementation so they will require long-term follow-
up by an endocrinologist.
In the acute phase, the first priority is to stabilize the BP. Cortisol deficiency can cause severe
hypotension.
Treatment requires IV fluids (normal saline or dextrose if patient is hypoglycemic) and IV
hydrocortisone (or dexamethasone if there is significant swelling in the brain).
Final Diagnosis
Pituitary apoplexy
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9
Gastroenterology
Case 1
Chief Complaint
“My belly is swollen and it hurts.”
History and Physical Examination
A 58-year-old woman comes to the emergency department with fever, abdominal pain,
and abdominal distention. In the last several months, she has developed ascites, anorexia,
and progressive wasting. She also complains of severe itching. She is on no medications.
She is a former IV drug user who was discharged several months ago from an alcohol-
detoxification unit.
She is disheveled-appearing and cachectic with a grossly distended abdomen. Her T is
38.3 C (101.0 F), BP 110/70 mm Hg, pulse 107/min, and respirations 22/min. Physical
examination shows poor dentition, parotid gland enlargement, and scleral icterus. Her
lungs are clear and the heart has a RRR. The abdomen is distended, tympanitic, tender,
and with shifting dullness. A liver edge is not palpable, but the spleen is palpable 3 cm
below the left costal margin. Bilateral palmar erythema is noted. Multiple spider
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angiomata and excoriations are also present. A flapping tremor is noted when the patient
is asked to extend her wrists while her arms are outstretched.
Differential Diagnosis
Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
Alcoholic cirrhosis1.
More likely, as patient has signs of chronic liver disease and was recently
discharged from alcoholic detoxification center
—
Chronic viral hepatitis or acute hepatitis2.
Could be a possible diagnosis, given that the most common cause of cirrhosis in the
United States is hepatitis C (especially since patient is prior IV drug user and in an
age group with high rates of infectivity, i.e., baby boomer generation)
—
Spontaneous bacterial peritonitis3.
Must be ruled out in all patients who present with fever and ascites; however given
the lack of abdominal pain it is less likely
—
Peritoneal carcinomatosis secondary to ovarian cancer4.
Must be considered as an alternative source of ascites in a female patient—
PT, PTT, INR
CBC, peripheral smear
BUN/creatinine
Aspartate aminotransferase (AST)
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Test Results
Assessment
This patient has stigmata of chronic liver disease or cirrhosis. Signs of chronic liver disease on
physical examination include ascites, spider angiomata, caput medusa, splenomegaly, palmar
erythema, and asterixis (a flapping tremor when the wrists are extended), which this patient
has.
CLINICAL PEARL
Alanine aminotransferase (ALT)
Alkaline phosphatase
Total and fractionated bilirubin
Albumin
Total protein
PT 16 sec (normal <13 sec), PTT 38 sec, INR 1.4
WBCs 4,800/mm
3
, hemoglobin 11 mg/dL, platelets 120,000/mm
3
, MCV 102 mm
3
;
acanthocytosis on peripheral smear
BUN/creatinine 30 mg/dL, 1.0 mg/dL
AST 200 U/L
ALT 100 U/L (normal: 8–20 U/L)
Alkaline phosphatase 150 U/L (normal: 20–70 U/L)
Total bilirubin 3.4 mg/dL (normal: 0.1–1.0 mg/dL)
Albumin 2.8 g/dL (normal: 3.5–5.5 g/dL)
Total protein 6.5 g/dL (normal: 6–7.8 g/dL)
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Elevated arterial or free venous serum ammonia is the classic lab abnormality for
hepatic encephalopathy. Ammonia level does not, however, correlate with the degree
of hepatic encephalopathy.
The patient’s lethargy is indicative of hepatic encephalopathy but the neurolgic findings can
range from confusion, irritability to obtundance and personality change. Also common in
hepatic encephalopathy is a reversal of the sleep-wake cycle.
In liver disease, the Child-Pugh score helps to delineate prognosis.
Parameter 1 point 2 points 3 points
Total bilirubin, μmol/l
(mg/dL)
<2 2–3 >3
Serum albumin, g/dL >3.5 2.8–3.5 <2.8
PT INR <1.7 1.71–2.30 >2.30
Ascites None Mild Moderate to
severe
Hepatic encephalopathy None Grade I–II (or suppressed with
medication)
Points Class 1-yr survival
5–6 A 99%
7–9 B 81%
10–15 C 45%
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CLINICAL PEARL
Beware of the female patient who has a history of significant alcohol abuse and
presents with new ascites. She may have alcoholic liver cirrhosis, but you should also
consider ovarian cancer with peritoneal carcinomatosis. Ovarian cancer causing
ascites will have a low albumin gradient, indicating no evidence of portal
hypertension.
Basic Science Correlate
In portal hypertension, portosystemic shunting allows thiols, dimethyl sulfide, and
trimethylamine to pass into the lungs and be breathed out. These compounds lead to
the odor of fetor hepaticus (sweet, feces).
Spider angiomata are vascular lesions with a central arteriole surround by smaller
vessels and occur due to a rise in estradiol. The liver normally clears estradiol.
Palmar erythema is due to vasodilation due to increased estrogen.
Gynecomastia also occurs from an increase in free estradiol.
Caput medusa occurs when blood from the portal venous system is shunted through
the periumbilical veins and ultimately to the abdominal wall veins. This can lead to
a Cruveilhier-Baumgarten murmur.
PT and PTT elevations are due to a lack of clotting factor production (clotting
factors made in the liver).
The only clotting factors not made in the liver are von Willebrand’s factor and factor
VIII.
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This patient has a history of alcoholism, and the increase in AST when compared with ALT
points to alcohol-related liver disease. Chronic viral hepatitis should be ruled out given the
history of IV drug use. Serologies for hepatitis B and C should be performed. Hepatitis A does
not cause chronic liver disease, but an acute infection can be particularly severe when there is
underlying chronic hepatitis, and may lead to fulminant failure.
In a patient with or without a history of alcohol abuse who has ascites, always consider cancer
and tuberculosis as a potential etiology of the ascites. Vascular causes of ascites are less likely
in this case but may be ruled out through the use of Doppler U/S or CT of the abdomen with
contrast.
CLINICAL PEARL
The most common cause of cirrhosis in the United States is hepatitis C, followed by
alcoholic liver disease.
Other improbable causes of cirrhosis are primary biliary cirrhosis, hemochromatosis, Wilson
disease, and alpha 1-antitrypsin deficiency. These diseases should be ruled out in this patient,
given that they may be reversible. A thorough history should be obtained to rule out drug-
related hepatotoxicity secondary to isoniazid, methotrexate, or acetaminophen.
CLINICAL PEARL
Paracentesis should always be attempted, even if an obvious cause of liver disease is
assumed. The most important tests to do with the paracentesis fluid are SAAG and
WBC. A patient with cirrhosis and ascites is at high risk for the development of
479
spontaneous bacterial peritonitis. In a febrile patient with ascites, perform a diagnostic
paracentesis to exclude this. Peritoneal fluid with absolute polymorphonuclear
leukocytes >250/mm
3
(or total WBC 500/mm
3
) suggests the presence of infection.
Liver-generated ascites is a sign of advanced disease and usually results from portal
hypertension, which leads to vasodilatation. The vasodilatation that occurs triggers renal
sodium retention and results in high intravascular volume and ascites formation. The
volume/pressor sensors in the cirrhotic patient are limited in the face of volume overload.
Consequently, these volume/pressure sensors sense volume depletion in the face of volume
overload and paradoxically stimulate release of renin/aldosterone, which leads to more
increased sodium retention and increased fluid volume.
Other causes of progressive ascites include malignant ascites (e.g., ovarian carcinoma), right-
sided heart failure, and vascular obstruction due to hepatic vein thrombosis (Budd-Chiari) or
inferior vena cava thrombosis.
The etiology of ascites can be distinguished by obtaining a serum ascites-albumin gradient
(SAAG). This is a gradient obtained by taking the difference between the serum albumin and
the albumin in the ascitic fluid.
A serum ascites-albumin difference of >1.1 g/dL is indicative of portal hypertension and is
seen in cirrhosis, cardiovascular ascites (congestive heart failure), or hepatic/portal vein
thrombosis syndromes. If the serum ascites albumin gradient (SAAG) is <1.1, portal
hypertension is absent; this can be seen in peritoneal carcinomatosis, peritonitis in the absence
of cirrhosis (i.e., tuberculosis), nephrotic syndrome, or pancreatic or biliary ascites. Basically,
if the ascitic fluid albumin level is much lower than the serum albumin level, it is from a
hydrostatic problem like portal hypertension.
SAAG (gm/dL) consistent with carcinomatosis, tuberculosis, pancreatitis, serositis, or
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