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Acute hepatic failure

2016-05-26T20:03:49Z

Diana.coleman: spelling changes

==Definitions<ref>O’Grady, JG, Schalm SW, Williams R. Acute liver failure: redefining the syndromes. Lancet. July 1993, Volume 342, Issue 8866, Page 273-275</ref>==
*Hyperacute liver failure: encephalopathy occurs within 7 days of the onset of jaundice; this subset is likely to survive with medical management despite the high incidence of cerebral edema
*Acute liver failure: interval of 8-28 days from jaundice to encephalopathy; this subset has a high incidence of cerebral edema and a poorer prognosis without liver transplant
*Subacute liver failure: interval of 5-12 weeks from the onset of jaundice to the onset of encephalopathy; this subset has a lower incidence of cerebral edema, but a poor prognosis

==Causes==
===Acetaminophen Toxicity===
*Now the most common cause of acute liver failure in the US<ref>Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States. Ann Intern Med. 2002 Dec 17; 137(12): 947-54.</ref>
*Small amount of Acetaminophen is metabolized by Cytochrome P450 into NAPQI, which is a toxic metabolite
*In therapeutic doses, NAPQI combines rapidly with glutathione to form nontoxic metabolites that are excreted in the urine
*In overdose, glutathione stores are used up and NAPQI binds to cell proteins in the liver which leads to cell death
*See [[Acetaminophen toxicity]]

===Viral Hepatitis===
*Hepatocellular pattern of injury, where AST and ALT are higher than Tbili and Alk Phos; likely to have significantly elevated ALT and AST (20x normal or higher)
*Of note, transmission of Hepatitis B and Hepatitis C through donated blood, blood products, and organs is rare in the US since blood screening became available in 1992
*Hepatitis A
**Fecal-oral transmission
**Associated with epidemics linked to a common source (water)
**Most common risk factor is travel outside of the US <ref>Oyama, LC: Disorders of the Liver and Biliary Tractin Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 107: p 1186-1204.</ref>
**Not associated with chronic carrier state; incubation period is approximately 30 days, and infectivity usually resolved prior to symptom onset
*Hepatitis B
**Transmitted parenterally, blood contact, and unprotected sex
**90% of exposed infants progress to chronic hepatitis; 10% of exposed adults progress to chronic hepatitis
**Serology<ref> www.cdc.gov/hepatitis </ref>
{| {{table}}
| align="center" style="background:#f0f0f0;"|'''Clinical Scenario'''
| align="center" style="background:#f0f0f0;"|'''HBsAg'''
| align="center" style="background:#f0f0f0;"|'''anti-HBc'''
| align="center" style="background:#f0f0f0;"|'''anti-HBs'''
|-
| Susceptible to infection||negative||negative||negative
|-
| Immune due to natural infection||negative||positive||positive
|-
| Immune due to Hep B infection||negative||negative||positive
|-
| Acutely infected||positive||anti-HBc- positive; IgM anti-HBc- positive||negative
|-
| Chronically infected||positive||anti-HBc- positive; IgM anti-HBc- negative||negative
|}
*Hepatitis C
**Transmitted through IV drug use (most common) and infrequently through sexual contact
**90% of HCV infections progress to chronic hepatitis<ref>Oyama, LC: Disorders of the Liver and Biliary Tractin Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 107: p 1186-1204</ref>
*Hepatitis D
**Transmission similar to Hepatitis B
**Can only co-infect patients with Hepatitis B (actively producing HBsAg)
**Presentation can range from acute self-limited disease to fulminant hepatitis or chronic infection
*Hepatitis E
**Fecal-oral transmission
**Usually results in mild illness, but can cause fulminant hepatitis in pregnant women<ref>Rein DB, Stevens GA, Theaker J, Wittenborn JS, Wiersma ST. The Global Burden of Hepatitis E Virus Genotypes 1 and 2 in 2005. Hepatology, Vol. 55, No. 4, 2012: 988-997</ref>
===Alcohol-related Liver Disease===
*Presentation can range from mild abdominal pain, nausea and vomiting to acute liver failure
*May have large palpable liver from fatty infiltration, or may have small nonpalpable liver 2/2 cirrhosis from chronic disease
*Will have moderate elevations in AST and ALT (levels >10x normal are unusual)
**AST:ALT ration >2 is typical
*May also have electrolyte abnormalities from malnutrition or alcoholic/starvation ketoacidosis
===Drug or Toxin Related Liver Disease===
*Liver damage from drugs or toxins may be cytotoxic from the primary drug or its metabolites, or may be caused by veno-occlusive disease or hypersensitivity disease<ref>Oyama, LC: Disorders of the Liver and Biliary Tractin Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 107: p 1186-1204</ref>
*Common Drugs and Toxins
**Acetaminophen
**Amiodarone
**Amphotericin
**Anabolic steroids
**Azathioprine
**Carbamazepine
**Chlorpromazine
**Cisplatin
**Contraceptives
**Cyclophosphamide
**Erythromycin
**Gold salts
**Haloperidol
**Isoniazid
**Ketoconazole
**Lovastatin
**Methotrexate
**Methoxyflurane
**Methyldopa
**Phenobarbital
**Phenytoin
**Quinidine
**Salicylates
**Tetracycline
**Valproic acid
**Verapamil
===Other Rare Causes of Acute Liver Failure===
*'''Wilson’s disease''': unexplained elevations in LFTs, neuro-psychiatric symptoms, Kayser-Fleischer rings on eye exam
*'''Auto-immune hepatitis''': more common in women, liver disease without explanation, may have family history of other autoimmune disorders
*'''Hemochromatosis''': family history of liver disease and cardiac disease
*'''Budd-Chiari''': history of hypercoagulable disorder, abdominal pain, and ascites
*'''Viral infections''': HSV, Epstein-Barr, varicella-zoster, toxoplasmosis
==Clinical Features==
*Common findings in acute liver failure
**Tender hepatomegaly
**Jaundice
**Encephalopathy
**Asterixis
*Common findings in chronic liver failure
**Ascites
**Caput medusae
**Palmar erythema
**Spider angiomata
**Gynecomastia
**Testicular atrophy
**Parotid gland enlargement
**Muscular atrophy
**May also have jaundice, encephalopathy, and asterixis as in acute liver failure
==Differential Diagnosis==
*Encephalopathy (altered mental status)
**Hypoglycemia
**Hypoxia
**Intracerebral hemorrhage or mass
**Meningitis/encephalitis
**CVA
**Intoxication
**Myxedema coma
**Wernicke encephalopathy
**Sepsis
**Seizure/post-ictal state
**Uremia
**Electrolyte abnormality
*Jaundice
**Hepatitis
**Hemolysis
**Biliary pathology (CBD obstruction)
**Pregnancy
**Congenital diseases (more likely to present in early childhood)
*Ascites
**Hepatitis or cirrhosis
**Heart failure or constrictive pericarditis
**Malignancy (primary or metastatic peritoneal carcinoma)
**Pancreatitis
**Vasculitis
**Connective tissue disorders
**Chylous ascites
==Diagnosis==
===Labs===
*AST and ALT
**Enzymes found mainly in hepatic cells, though ALT is more specific to the liver than AST
**Extreme elevation in AST (>3000U/L, or >40x upper limit of normal) is consistent with acetaminophen toxicity or ischemic injury
**Moderate elevations (10-40x upper limit of normal) is consistent with viral hepatitis
**Mild elevations (<10x upper limit of normal) is consistent with alcoholic hepatitis
*Alkaline Phosphatase
**Found in bile canaliculi (but also in placenta, ileal mucosa, bone, and kidney)
**Elevated in diseases of cholestasis
**Rare for levels to be >3x normal limit in acute liver failure
*Bilirubin
**Elevated in diseases of cholestasis
**In obstructive diseases, the direct bilirubin will usually be about 50% of the total bilirubin; if indirect bilirubin is higher, more suggestive of hemolysis or problem with conjugation
*Coagulation Studies
**Reflects the liver’s ability to synthesize clotting factors
**INR >6.5 or PT >20 seconds indicates patients at high risk for death
*Albumin
**Reflects synthetic function of the liver
**Has a long half-life (20 days) and may not be decreased early in disease
*Ammonia
**Elevated as a result of impaired clearance
**Poor correlation between degree of elevation and severity of encephalopathy symptoms
*Chemistry Panel
**Electrolyte abnormalities may indicate malnutrition or dehydration
**Creatinine is used as a prognostic indicator
**Need to check a glucose because patients with liver failure are prone to hypoglycemia
*CBC
**Not useful in diagnosing the cause of liver failure, but helpful in determining coexisting infection, anemia, thrombocytopenia
*Hepatic Viral Serologies
**Consider for all patients with undifferentiated liver failure
**IgM anti-HBc may be the only positive marker in acute Hepatitis B infection
**Anti-HCV and HCV RNA are present in both chronic and acute Hepatitis C infections, so it is difficult to differentiate based on serologies, but presence of HCV RNA in the absence of anti-HCV is more suggestive of acute infection<ref>Bailey, C, Hern HG. Hepatic Failure: An Evidence-Based Approach In The Emergency Department. Emergency Medicine Practice. Vol. 12, No. 4, 2014.</ref>
**Only need to test for IgM anti-HEV in patients who are symptomatic and have just travelled from areas where Hepatitis E is endemic
===Imaging===
*Consider US or CT in patients with jaundice to evaluate for a mechanical obstruction
*Otherwise, tailor imaging towards specific complaints
==Treatment==
*Treatment is mostly supportive and tailored towards the specific etiology
*Early consideration regarding transporting patient to a transplant center given potential for rapid deterioration
*Symptom specific supportive treatment options
**Encephalopathy: consider lactulose of neomycin
**Seizures: consider phenytoin over benzodiazepines (prevent benzodiazepine oversedation secondary to decreased hepatic clearance)
**Intracranial Hypertension: elevated head of bed, mannitol, short-term hyperventilation; hypothermia may be a bridge to transplant; no benefit from steroids
**Coagulopathy
***Prophylactic normalization of the INR is not necessary unless procedure (such as paracentesis) is planned; then can give Vitamin K
***Recommend platelet transfusion to 10K for asymptomatic patients, and to 50-70K for patients undergoing invasive procedures
**See [[Acetaminophen (Tylenol) toxicity]] for specifics regarding treatment of acetaminophen toxicity
**See [[Spontaneous Bacterial Peritonitis]] for specifics regarding diagnosis and treatment of SBP
==Disposition==
*Admission to ICU with early consideration for transportation to transplant center
==References==
<references/>

Acute hepatic failure

2016-05-16T19:25:43Z

Diana.coleman: Created page with "==Definitions<ref>O’Grady, JG, Schalm SW, Williams R. Acute liver failure: redefining the syndromes. Lancet. July 1993, Volume 342, Issue 8866, Page 273-275</ref>== *Hyperac..."

==Definitions<ref>O’Grady, JG, Schalm SW, Williams R. Acute liver failure: redefining the syndromes. Lancet. July 1993, Volume 342, Issue 8866, Page 273-275</ref>==
*Hyperacute liver failure: encephalopathy occurs within 7 days of the onset of jaundice; this subset is likely to survive with medical management despite the high incidence of cerebral edema
*Acute liver failure: interval of 8-28 days from jaundice to encephalopathy; this subset has a high incidence of cerebral edema and a poorer prognosis without liver transplant
*Subacute liver failure: interval of 5-12 weeks from the onset of jaundice to the onset of encephalopathy; this subset has a lower incidence of cerebral edema, but a poor prognosis

==Causes==
===Acetaminophen Toxicity===
*Now the most common cause of acute liver failure in the US<ref>Ostapowicz G, Fontana RJ, Schiodt FV, et al. Results of a prospective study of acute liver failure at 17 tertiary care centers in the United States. Ann Intern Med. 2002 Dec 17; 137(12): 947-54.</ref>
*Small amount of Acetaminophen is metabolized by Cytochrome P450 into NAPQI, which is a toxic metabolite
*In therapeutic doses, NAPQI combines rapidly with glutathione to for nontoxic metabolites that are excreted in the urine
*In overdose, glutathione stores are used up and NAPQI binds to cell proteins in the liver which leads to cell death
*See [[Acetaminophen (Tylenol) toxicity]]
===Viral Hepatitis===
*Hepatocellular pattern of injury, where AST and ALT are higher than Tbili and Alk Phos; likely to have significantly elevated ALT and AST (20x normal or higher)
*Of note, transmission of Hepatitis B and Hepatitis C through donated blood, blood products, and organs is rare in the US since blood screening became available in 1992
*Hepatitis A
**Fecal-oral transmission
**Associated with epidemics linked to a common source (water)
**Most common risk factor is travel outside of the US <ref>Oyama, LC: Disorders of the Liver and Biliary Tractin Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 107: p 1186-1204.</ref>
**Not associated with chronic carrier state; incubation period is approximately 30 days, and infectivity usually resolved prior to symptom onset
*Hepatitis B
**Transmitted parenterally, blood contact, and unprotected sex
**90% of exposed infants progress to chronic hepatitis; 10% of exposed adults progress to chronic hepatitis
**Serology<ref> www.cdc.gov/hepatitis </ref>
{| {{table}}
| align="center" style="background:#f0f0f0;"|'''Clinical Scenario'''
| align="center" style="background:#f0f0f0;"|'''HBsAg'''
| align="center" style="background:#f0f0f0;"|'''anti-HBc'''
| align="center" style="background:#f0f0f0;"|'''anti-HBs'''
|-
| Susceptible to infection||negative||negative||negative
|-
| Immune due to natural infection||negative||positive||positive
|-
| Immune due to Hep B infection||negative||negative||positive
|-
| Acutely infected||positive||anti-HBc- positive; IgM anti-HBc- positive||negative
|-
| Chronically infected||positive||anti-HBc- positive; IgM anti-HBc- negative||negative
|}
*Hepatitis C
**Transmitted through IV drug use (most common) and infrequently through sexual contact
**90% of HCV infections progress to chronic hepatitis<ref>Oyama, LC: Disorders of the Liver and Biliary Tractin Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 107: p 1186-1204</ref>
*Hepatitis D
**Transmission similar to Hepatitis B
**Can only co-infect patients with Hepatitis B (actively producing HBsAg)
**Presentation can range from acute self-limited disease to fulminant hepatitis or chronic infection
*Hepatitis E
**Fecal-oral transmission
**Usually results in mild illness, but can cause fulminant hepatitis in pregnant women<ref>Rein DB, Stevens GA, Theaker J, Wittenborn JS, Wiersma ST. The Global Burden of Hepatitis E Virus Genotypes 1 and 2 in 2005. Hepatology, Vol. 55, No. 4, 2012: 988-997</ref>
===Alcohol-related Liver Disease===
*Presentation can range from mild abdominal pain, nausea and vomiting to acute liver failure
*May have large palpable liver from fatty infiltration, or may have small nonpalpable liver 2/2 cirrhosis from chronic disease
*Will have moderate elevations in AST and ALT (levels >10x normal are unusual)
**AST:ALT ration >2 is typical
*May also have electrolyte abnormalities from malnutrition or alcoholic/starvation ketoacidosis
===Drug or Toxin Related Liver Disease===
*Liver damage from drugs or toxins may be cytotoxic from the primary drug or its metabolites, or may be caused by veno-occlusive disease or hypersensitivity disease<ref>Oyama, LC: Disorders of the Liver and Biliary Tractin Marx JA, Hockberger RS, Walls RM, et al (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 8. St. Louis, Mosby, Inc., 2014, (Ch) 107: p 1186-1204</ref>
*Common Drugs and Toxins
**Acetaminophen
**Amiodarone
**Amphotericin
**Anabolic steroids
**Azathioprine
**Carbamazepine
**Chlorpromazine
**Cisplatin
**Contraceptives
**Cyclophosphamide
**Erythromycin
**Gold salts
**Haloperidol
**Isoniazid
**Ketoconazole
**Lovastatin
**Methotrexate
**Methoxyflurane
**Methyldopa
**Phenobarbital
**Phenytoin
**Quinidine
**Salicylates
**Tetracycline
**Valproic acid
**Verapamil
===Other Rare Causes of Acute Liver Failure===
*'''Wilson’s disease''': unexplained elevations in LFTs, neuro-psychiatric symptoms, Kayser-Fleischer rings on eye exam
*'''Auto-immune hepatitis''': more common in women, liver disease without explanation, may have family history of other autoimmune disorders
*'''Hemochromatosis''': family history of liver disease and cardiac disease
*'''Budd-Chiari''': history of hypercoagulable disorder, abdominal pain, and ascites
*'''Viral infections''': HSV, Epstein-Barr, varicella-zoster, toxoplasmosis
==Clinical Features==
*Common findings in acute liver failure
**Tender hepatomegaly
**Jaundice
**Encephalopathy
**Asterixis
*Common findings in chronic liver failure
**Ascites
**Caput medusae
**Palmar erythema
**Spider angiomata
**Gynecomastia
**Testicular atrophy
**Parotid gland enlargement
**Muscular atrophy
**May also have jaundice, encephalopathy, and asterixis as in acute liver failure
==Differential Diagnosis==
*Encephalopathy (altered mental status)
**Hypoglycemia
**Hypoxia
**Intracerebral hemorrhage or mass
**Meningitis/encephalitis
**CVA
**Intoxication
**Myxedema coma
**Wernicke encephalopathy
**Sepsis
**Seizure/post-ictal state
**Uremia
**Electrolyte abnormality
*Jaundice
**Hepatitis
**Hemolysis
**Biliary pathology (CBD obstruction)
**Pregnancy
**Congenital diseases (more likely to present in early childhood)
*Ascites
**Hepatitis or cirrhosis
**Heart failure or constrictive pericarditis
**Malignancy (primary or metastatic peritoneal carcinoma)
**Pancreatitis
**Vasculitis
**Connective tissue disorders
**Chylous ascites
==Diagnosis==
===Labs===
*AST and ALT
**Enzymes found mainly in hepatic cells, though ALT is more specific to the liver than AST
**Extreme elevation in AST (>3000U/L, or >40x upper limit of normal) is consistent with acetaminophen toxicity or ischemic injury
**Moderate elevations (10-40x upper limit of normal) is consistent with viral hepatitis
**Mild elevations (<10x upper limit of normal) is consistent with alcoholic hepatitis
*Alkaline Phosphatase
**Found in bile canaliculi (but also in placenta, ileal mucosa, bone, and kidney)
**Elevated in diseases of cholestasis
**Rare for levels to be >3x normal limit in acute liver failure
*Bilirubin
**Elevated in diseases of cholestasis
**In obstructive diseases, the direct bilirubin will usually be about 50% of the total bilirubin; if indirect bilirubin is higher, more suggestive of hemolysis or problem with conjugation
*Coagulation Studies
**Reflects the liver’s ability to synthesize clotting factors
**INR >6.5 or PT >20 seconds indicates patients at high risk for death
*Albumin
**Reflects synthetic function of the liver
**Has a long half-life (20 days) and may not be decreased early in disease
*Ammonia
**Elevated as a result of impaired clearance
**Poor correlation between degree of elevation and severity of encephalopathy symptoms
*Chemistry Panel
**Electrolyte abnormalities may indicate malnutrition or dehydration
**Creatinine is used as a prognostic indicator
**Need to check a glucose because patients with liver failure are prone to hypoglycemia
*CBC
**Not useful in diagnosing the cause of liver failure, but helpful in determining coexisting infection, anemia, thrombocytopenia
*Hepatic Viral Serologies
**Consider for all patients with undifferentiated liver failure
**IgM anti-HBc may be the only positive marker in acute Hepatitis B infection
**Anti-HCV and HCV RNA are present in both chronic and acute Hepatitis C infections, so it is difficult to differentiate based on serologies, but presence of HCV RNA in the absence of anti-HCV is more suggestive of acute infection<ref>Bailey, C, Hern HG. Hepatic Failure: An Evidence-Based Approach In The Emergency Department. Emergency Medicine Practice. Vol. 12, No. 4, 2014.</ref>
**Only need to test for IgM anti-HEV in patients who are symptomatic and have just travelled from areas where Hepatitis E is endemic
===Imaging===
*Consider US or CT in patients with jaundice to evaluate for a mechanical obstruction
*Otherwise, tailor imaging towards specific complaints
==Treatment==
*Treatment is mostly supportive and tailored towards the specific etiology
*Early consideration regarding transporting patient to a transplant center given potential for rapid deterioration
*Symptom specific supportive treatment options
**Encephalopathy: consider lactulose of neomycin
**Seizures: consider phenytoin over benzodiazepines (prevent benzodiazepine oversedation secondary to decreased hepatic clearance)
**Intracranial Hypertension: elevated head of bed, mannitol, short-term hyperventilation; hypothermia may be a bridge to transplant; no benefit from steroids
**Coagulopathy
***Prophylactic normalization of the INR is not necessary unless procedure (such as paracentesis) is planned; then can give Vitamin K
***Recommend platelet transfusion to 10K for asymptomatic patients, and to 50-70K for patients undergoing invasive procedures
**See [[Acetaminophen (Tylenol) toxicity]] for specifics regarding treatment of acetaminophen toxicity
**See [[Spontaneous Bacterial Peritonitis]] for specifics regarding diagnosis and treatment of SBP
==Disposition==
*Admission to ICU with early consideration for transportation to transplant center
==References==
<references/>

Large bowel obstruction

2016-03-11T21:30:38Z

Diana.coleman:

==Background==
*Much less common than SBO, but more ominous (frequently associated with malignancy)
*Most commonly occurs in the left colon
*Causes
**Cancer
***Obstruction originating from the left colon is likely to manifest with symptoms earlier than obstruction originating from the right colon, because the lumen from the descending colon and the sigmoid is smaller.
**Adhesions
**Volvulus
**Diverticular disease
**Fecal impaction
**Strictures
**Hernias
**Pseudo-obstruction (Ogilvie's Syndrome)

==Clinical Features==
*Abdominal pain
*Abdominal distension
**Distension is greater if the ileocecal valve is competent (it creates a closed loop obstruction). If the ileocecal valve is not competent, you are more likely to see some dilation of the small bowel as well <ref name="Radiology"> Jaffe T, Thompson WM. Large-Bowel Obstruction in the Adult: Classic Radiographic and CT Findings, Etiology, and Mimics. Radiology. 2015; 275(3):651-663 </ref>
*Obstipation
*Vomiting
*Palpable abdominal mass (could be distended bowel or could be tumor causing obstruction)
*Fever and tachycardia should prompt investigation for gangrene and perforation

==Differential Diagnosis==
Other causes of abdominal pain, distension, obstipation (similar to the causes of LBO):
*SBO
**More likely to have an abrupt onset with SBO, whereas patients with LBO are more likely to be elderly and with insidious onset
*Colorectal cancer
*Diverticulitis
*Volvulus
*Adhesions
*Fecal impaction
*Gallstone ileus
*Inflammatory Bowel Disease

==Diagnosis==
*Labs
**None are diagnostic
**Check electrolytes to assess for dehydration
**Leukocytosis could indicate gangrene or perforation
**Anemia could indicate malignancy as source of obstruction
**ABG may help assess if the patient has respiratory compromise from diaphragmatic compression <ref name="surgclinic"> Lopez-Kostner F, Hool GR, et al. Management and Causes of Acute Large-Bowel Obstruction.. Surgical Clinics of North America. 1997; 77(6); 1265-1290 </ref>
*Imaging <ref name="radclinic"> Murphy K, Twomey M, McLaughlin P, et al. Imaging of Ischemia, Obstruction and Infection in the Abdomen. Radiology Clinics of North America. 2105; 53: 847-869 </ref>
**XR
***Sensitivity of 69% to 80% for detecting bowel obstruction, but insensitive for diagnosing cause or location
***Upright films can detect pneumoperitoneum, hollow viscus perforation
***Distended colon (small bowel may appear distended as well if the ileocecal valve is competent)
***Cecal diameter of ≥12cm is associated with higher risk of perforation
**CT
***Can usually identify the cause of obstruction, except in cases of pseudo-obstruction
***Sensitivity for diagnosing large bowel obstruction as high as 90% (not as high as for small bowel obstruction)
***Can also diagnose intestinal ischemia
**Colonoscopy
***Can be used to rule-out pseudo-obstruction in patients who are not candidates for urgent surgical intervention

==Management==
*Rehydration
*NPO status
*Pain management
*Gastric decompression with NGT if pt has significant vomiting or evidence of small bowel distension
*Antibiotics if gangrene or perforation is suspected (need gram-negative and anaerobic coverage)

'''Treatment of specific etiologies of LBO'''
*Diverticular Abscess: percutaneous drainage
*Volvulus: endoscopic decompression
*Pseudo-obstruction: endoscopic decompression
*Intussusception: surgical intervention

==Disposition==
*Admission for rehydration/resuscitation
*Appropriate consultation (GI, surgery, IR)

==See Also==
*[[Small Bowel Obstruction (SBO)]]
*[[Ogilvie's Syndrome]]

==References==
<references/>