Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3063_Библиотеки_им_академика_М_И_Перельмана
.pdf
<1.1 nephrosis
SAAG (gm/dL)
≥1.1
consistent with portal hypertension, CHF, or Budd-Chiari syndrome
The liver has a large role in synthesis of albumin and proteins involved in coagulation.
Laboratory abnormalities of cirrhosis include evidence of poor synthetic function demonstrated
by low serum albumin levels and elevated PT and PTT. Elevation of the PT and PTT is caused
by deficient production of clotting factors, which results from loss of liver parenchymal cell
function. Vitamin K serves as a cofactor used by liver parenchymal cells in the production of
these clotting factors. Other hematologic abnormalities seen in cirrhosis include anemia and
thrombocytopenia from hypersplenism, marrow suppression, or the anemia of chronic disease.
Liver failure is often associated with an elevation in the direct bilirubin, transaminases, lactate
dehydrogenase, and alkaline phosphatase. However, patients with a cirrhotic liver that
becomes progressively more fibrotic may lose their ability to produce these enzymes, and,
consequently, their levels can be normal.
CLINICAL PEARL
When sudden worsening of ascites occurs in a patient with cirrhosis, you have to
consider hepatoma, spontaneous bacterial peritonitis, and viral hepatitis. A repeat
paracentesis is mandatory to exclude spontaneous bacterial peritonitis.
Hepatoma can be evaluated through diagnostic imaging such as ultrasonography or CT
scan, as well as serum alphafetoprotein (which is elevated with hepatoma).
481
Further Tests/Results
Hepatitis B and C serologies Negative
Paracentesis WBCs 50 mm
3
; Gram stain and culture negative; albumin 1.2
Fe (iron) studies Normal
Ceruloplasmin levels Normal
Alpha-1 antitrypsin levels Normal
Antimitochondrial antibodies Negative
Liver U/S mass Shrunken nodular fatty liver; normal bile ducts; no evidence of mass
CLINICAL PEARL
Fever + abdominal + cirrhosis = SBP must be ruled out.
Further Management
Salt restriction, diuretics (spironolactone and furosemide)
Counsel against further alcohol ingestion and encourage enrollment in alcohol treatment
program
Balanced diet with adequate protein ingestion; possible use of diet-enriched branched chain
amino acids to protect against development of hepatic encephalopathy
Follow patient closely and watch for signs of GI bleed and encephalopathy
Given that patient has portal hypertension and ascites, upper endoscopy to exclude
esophageal varices
482
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Basic Science Correlate
Discussion
This patient presents with several classic findings of cirrhosis secondary to alcoholic liver
disease. The other disease entities in the differential have been ruled out by negative testing.
Alcoholic hepatitis may present with acute symptoms of fever, hepatosplenomegaly, and
elevated transaminases. In alcoholic cirrhosis, patients usually present with anorexia, loss of
muscle mass, and fatigue. The liver may be enlarged and fatty, but as the disease progresses,
cirrhosis develops and the liver becomes hard, nodular, shrunken, and scarred. Fibrous bands
connecting portal triads and central veins, as well as regenerative parenchyma-forming
micronodules, characterize liver histology in cirrhosis.
Given that patient has hepatic encephalopathy, lactulose and rifaximin are advisable
Spironolactone, a direct aldosterone antagonist, can lead to gynecomastia and
hyperkalemia
Furosemide, a loop diuretic, inhibits Na-K-2Cl symporter in the thick ascending
limb of the loop of Henle and can lead to hypokalemia
Lactulose is a non-digestible disaccharide that reduces the ammonia levels through
increased bowel movements. It is titrated until the patient has 2–3 bowel movements
per day. Dehydration is a common side effect
Rifaximin interferes with transcription by binding to the γ-subunit of bacterial RNA
polymerase. This reduces relapse of hepatic encephalopathy and improves quality of
life.
483
Men often present with gynecomastia and testicular atrophy caused by decreased hepatic
clearance of androstenedione that is converted to estrogen and leads to increased estrogen
levels. Patients with alcoholic cirrhosis usually have signs of portal hypertension, which
include ascites, hemorrhoids, splenomegaly, and esophageal varices.
Transaminase elevations are usually mild and do not exceed 300 U/L. The transaminase
elevation is characterized by an AST that is approximately 2 to 3x ALT, as is seen here.
Bilirubin elevations are often modest but progress as the disease worsens. Patients have
decreased albumin levels and oncotic pressure, which increase the risk of ascites formation.
Splenomegaly can be associated with pancytopenia. Coagulopathy is another sign of liver
dysfunction. Hepatic encephalopathy is seen in end-stage disease (to be discussed in a later
case).
Patients with alcoholic fatty liver have a good prognosis, and the problem may resolve after
cessation of drinking. Patients with alcoholic hepatitis who stop drinking rarely develop
cirrhosis. Of those who continue drinking, the incidence of cirrhosis is 45–80%.
Hyperbilirubinemia, prolongation of clotting times, ascites, and encephalopathy are associated
with a mortality, which may exceed 50%. Prognosis is largely determined by whether the
patient continues to drink. In a large study from Copenhagen, the 5-year survival for
nondrinkers without jaundice was 85%, whereas it was only 60% for those who drank. Once
jaundice occurs, survival falls to 50% in nondrinkers and 30% in drinkers. GI bleed carries the
worst prognosis.
Treatment is largely supportive. Corticosteroids may be used in treatment of acute alcoholic
hepatitis in patients who are very coagulopathic, but corticosteroids play no role in treatment
once cirrhosis occurs. Advanced disease can be treated with liver transplantation if the patient
discontinues drinking.
Follow-up Management and Prevention
Patients should have surveillance for varices every 2 years if the initial scope was negative
484
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Final Diagnosis
Cirrhosis
If varices are present, band ligation is the most appropriate therapy
Prevention of variceal bleeds is with a nonselective beta blocker (propranolol, or nadolol)
If a patient has had spontaneous bacterial peritonitis, subsequent antibiotic prophylaxis with
norfloxacin is indicated
Patients with cirrhosis undergo surveillance for HCC with ultrasonography every 6 mos
485
Case 2
Chief Complaint
“I’m vomiting blood.”
History and Physical Examination
A 72-year-old man comes to the emergency department vomiting blood. The patient has a
known history of ethanol abuse and has had a couple of upper GI bleeds in the past. He
was on a drinking binge earlier today, and an hour ago he was found by the emergency
workers in a pool of blood on the sidewalk. He denies any pain at this time.
He is afebrile. His BP is 80 mm Hg/palpation and pulse 125/min. He is stuporous and
smells of alcohol. Physical examination shows scleral icterus, gynecomastia, and spider
angiomata. Cardiovascular examination is normal except for tachycardia. The chest is
clear to auscultation. The abdomen is soft, non-tender, and nondistended; splenomegaly is
evident. Rectal exam is significant for melena.
Differential Diagnosis
Bleeding esophageal varices
1.
The most likely diagnosis of upper GI bleed in patients with known cirrhosis or who
have stigmata of chronic liver disease
—
Mallory-Weiss tear
2.
Occurs most commonly in patients with a history of retching and vomiting; although
—
486
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Initial Management
Setting: emergency department
Diagnostic/Therapeutic Plan
In the case of upper GI bleed, the initial management plan is the same whatever the cause. It
always focuses on stabilizing the patient.
this patient did have an alcoholic binge earlier, there is no mention of vomiting or
retching
Erosive gastritis3.
A common finding in patients with alcoholism; however, less likely to cause severe
upper GI bleed and more likely to cause melena
—
Peptic ulcer bleeding4.
Caused by NSAIDs or H. pylori, which can cause upper GI bleed; however, in the
setting of chronic liver disease, the more likely cause is varices due to portal
hypertension
—
Insert 2 large-bore IV lines and start fluids (normal saline or crystalloid)
Continue saline infusion until systolic BP is >90 mm Hg, HR decreases <90/min, or urine
output (if affected) increases
—
Obtain a CBC, biochemical profile, and PT/PTT
Give transfusions of packed RBC as needed
Fresh frozen plasma in patients with coagulopathy—
May require urgent upper endoscopy and therapeutic intervention
Insert a nasogastric tube to determine if there is ongoing, active bleeding
487
Test Results
CLINICAL PEARL
Upper GI bleed can manifest as hematemesis, melena, hematochezia, or hemodynamic
changes (dizziness).
Assessment
The patient presents with evidence of vomiting bright red blood and with melena in the rectal
vault. The presence of melena suggests a bleed greater than 100 mL, originating from a source
proximal to the ligament of Treitz.
Upper GI bleed in an alcoholic patient has several possible etiologies. Massive blood loss is
often caused by esophageal varices resulting from progressive portal hypertension. However,
even alcoholics with known esophageal varices often suffer upper GI bleed from other causes.
Other possibilities include peptic ulcer disease or severe gastritis. Recurrent retching can
result in a Mallory-Weiss tear and subsequent bleeding.
This patient also has evidence of cirrhosis and alcoholic liver disease on physical examination
(gynecomastia, spider angiomatas, icteric sclera) and lab findings (elevated bilirubin, elevated
Hemoglobin 10 mg/dL (normal 13–16 mg/dL)
Platelets 80,000/mm
3
(normal 140,000–340,000/mm
3
)
Sodium 150 mEq/L (normal 135–150 mEq/L), BUN 30 mg/dL (normal: 8–18 mg/dL),
creatinine 1.4 mg/dL (normal: 0.6–1.3 mg/dL)
Bilirubin 3.5 mg/dL (normal: 0.1–1.0 mg/dL), AST 240 U/L, ALT 80 U/L (normal: 8–20
U/L), alkaline phosphatase 160 U/L, PT/PTT: 17 sec/45 sec (elevated).
488
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
AST/ALT ratio 3:1, elevated PT/PTT, low albumin).
In assessing this patient, primary attention is given to determining the extent of blood loss and
stabilizing intravascular volume with crystalloids and packed RBC transfusions. Given the
history of alcoholism, evidence for an underlying coagulation defect should also be explored
and corrected. Emergent endoscopy should be performed to determine the source of bleeding
once the patient is stabilized.
CLINICAL PEARL
Because there is significant mortality and morbidity associated with upper GI bleed, an
upper endoscopy should be performed before discharge from the hospital. However,
nasogastric lavage showing bright blood (especially if the patient is hemodynamically
unstable) mandates an emergent consult with gastroenterology and endoscopy.
Further Management Plan/Results
Emergent upper
endoscopy once patient is
stabilized
Esophageal varices with cherry red spots and a varix with a clot but
no active bleeding; normal gastric mucosae with no evidence of peptic
ulcers
Banding of the esophageal
varices to control the
bleeding
CLINICAL PEARL
489
Nonselective beta-blockers (propranolol, nadolol) are the only effective treatment for
esophageal varices for first-time, as well as recurrent, bleeding.
Follow-up Management
Discussion
This patient has bleeding esophageal varices as a result of portal hypertension secondary to
alcohol-induced cirrhosis. Varices are portosystemic collaterals that can develop in the
esophagus, stomach, or rectum in patients with portal hypertension. Varices in the esophagus
and stomach can be seen in up to 60% of cirrhotic patients and have a 30% chance of bleeding.
Factors which increase the likelihood of variceal bleeding include size and presence of cherry
red spots or red streaks on varices. This patient had cherry red spots as well as a clot on a
varix that had recently bled.
About 60% of upper GI bleed in cirrhotics is caused by esophageal varices, while 7% is
caused by gastric varices. Variceal bleeding carries a high mortality rate of up to 70%.
Upper endoscopy is the mainstay of both diagnosis and treatment of varices. Octreotide should
be used immediately in all patients with variceal bleeding. Variceal rubber band ligation and
sclerotherapy are treatment options to control bleeding, but they do not treat portal
hypertension. Banding is used in patients with bleeding to prevent recurrent bleeding. Band
Admission to ICU for continued observation and blood transfusion as appropriate
1.
IV somatostatin/octreotide
2.
Monitor for signs of recurrent bleeding
3.
Propranolol once BP is stable
4.
Monitor for signs of delirium tremens
5.
Fresh frozen plasma if increased PT
6.
Norfloxacin as prophylaxis against SBP
7.
490
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Соседние файлы в папке Библиотека им академика М.И. Перельмана