Alcohol Abuse: Complications and Consequences
Alcoholism is a common substance-abuse disorder that affects virtually every organ system. Alcoholics are at increased risk for cirrhosis, gastrointestinal (GI) bleeding, pancreatitis, cardiomyopathy, trauma, mental health disorders (eg, depression, blackouts, dementia), and a wide variety of cancers. Patients frequently have poor insight into their addiction—a state commonly referred to as denial—and lack awareness of the short- and long-term complications of alcohol abuse.
The image shows a reticulin stain of liver tissue from an alcoholic with cirrhosis.
Alcohol Abuse: Complications and Consequences
Liver Disease and Associated Complications
Alcohol abuse is the second most common cause of cirrhosis in the United States, after hepatitis C.[1] Cirrhosis develops over many years of sustained abuse. Damage to the liver parenchyma from alcohol leads to progressive fibrosis, producing a nodular contour to the liver (white arrows). The scar tissue impairs portal vein blood flow,[2] which induces portal hypertension; this causes splenomegaly (yellow arrow), transudative ascites (red arrow), and varices. The computed tomography (CT) image shown demonstrates prominent esophageal varices (green arrow). Specialized multiphasic contrast-enhanced CT and magnetic resonance imaging (MRI) protocols can be used to assess the extent of liver disease and associated complications.[3]
Alcohol Abuse: Complications and Consequences
A 60-year-old woman presents for a new patient evaluation. She suffers from depression after the loss of her husband a year ago and admits to drinking approximately 60 g of alcohol daily. She recently presented to the emergency department (ED) for abdominal pain and underwent an abdominal CT scan (shown).
On review of her CT scan, which of the following changes could be attributed to her alcohol use?
- None; study is normal
- Alcoholic hepatic steatosis
- Alcoholic hepatitis
- Alcoholic cirrhosis
- Hepatocellular carcinoma (HCC)
Alcohol Abuse: Complications and Consequences
Answer: B. Alcoholic hepatic steatosis.
Ingestion of more than 60 g of alcohol daily causes morphologic changes to the liver. The first change is fatty replacement of the liver, or hepatic steatosis, due to an increase in fatty acids and glycerol 3-phosphate.[4]
On CT, the liver attenuation is lower (ie, darker) than the spleen (see the previous slide); on ultrasonography (US), the liver is more echogenic (ie, brighter) (red arrow) than the kidney (blue arrow); and on MRI, the liver loses signal on out-of-phase sequences. MRI is an excellent means of evaluating for subsequent complications such as portal hypertension, ascites, and HCC.[5] Newer imaging techniques, such as dual-energy CT, can quantify the degree of steatosis.[6] Hepatic steatosis is reversible, but if ingestion of alcohol is not decreased, it progresses to alcoholic hepatitis, followed by alcoholic cirrhosis.[7]
Alcohol Abuse: Complications and Consequences
Esophageal Damage
A 50-year-old man with a longstanding history of alcohol abuse and esophageal varices diagnosed on a recent esophagogram (shown) presents to the ED with hematemesis. The man was drinking heavily earlier in the day and started vomiting about 1 hour ago. The patient's initial vital signs show a heart rate of 90 beats/min, a blood pressure of 115/73 mm Hg, and a normal respiratory rate. While sitting in the waiting room, he has filled two cups with reddish fluid that contained blood.
After the administration of intravenous (IV) fluids, what is the most appropriate next step in management?
- Watchful waiting
- Repeat esophagogram
- CT of the chest, abdomen, and pelvis
- GI consult for endoscopy
- Interventional radiology consult for angiography
Alcohol Abuse: Complications and Consequences
Answer: D. GI consult for endoscopy.
The patient's history suggests either a bleeding esophageal varix or a Mallory-Weiss tear, both of which can be diagnosed and managed endoscopically.
Varices develop secondary to cirrhotic changes in the pressure and flow gradients of the liver vasculature. As varices grow, the risk of rupture and hemorrhage increases dramatically, with a 70% chance of rebleeding. Other clinical symptoms include blood in vomit; black, tarry, or bloody stools; lightheadedness; rapid heart rate; and loss of consciousness.[8]
In contrast, Mallory-Weiss tears are longitudinal mucosal lacerations at the esophagogastric junction or gastric cardia (shown) that develop from a sudden rise in intragastric pressure. The classic scenario involves a patient with protracted vomiting after alcoholic binge drinking who develops hematemesis. Hemodynamic instability and shock develop in as many as 10% of cases.
Endoscopy can differentiate varices from Mallory-Weiss tears and provide direct treatment. In some cases, surgery or angiotherapy is required to stop the bleeding.[9]
Alcohol Abuse: Complications and Consequences
Hepatocellular Carcinoma
HCC is one of the most common causes of cancer-related death, and roughly 30% of HCCs are due to excessive alcohol use.[10] In patients with 10 years of chronic alcohol abuse, the HCC risk is increased fivefold. Up to 75% of HCC are multifocal at diagnosis and the overall prognosis is poor, with a 5-year survival rate of 20.8%.[11] However, multiple treatment options are available for unresectable HCC, including transarterial chemoembolization, drug-eluting embolization, and radioembolization.[12] Patients at high risk for HCC can undergo US screening every 6 months.
Alcohol Abuse: Complications and Consequences
Esophageal Cancer
Alcohol use is one of the leading causes of esophageal cancer in the United States.[13] Among patients who drink more than 30 g of ethanol daily, the risk ratio for squamous cell carcinoma is 4.61 compared with abstainers. Dysphagia with solids and eventually with liquids is the most common presenting symptom of esophageal cancer. Endoscopy allows direct visualization and tissue biopsy. A barium swallow can show indirect signs of a mass lesion and provide functional information. The image shows a mid-esophageal endoluminal mass on barium swallow in a patient with esophageal cancer.
Surgical excision is the best option for curative therapy; nonoperative treatment is reserved for palliation of dysphagia. The overall 5-year relative survival rate for all stages of esophageal cancer is approximately 20% but the survival rate for late-stage cancer is about 5%.[14,15]
Alcohol Abuse: Complications and Consequences
Stroke
The brain CT scan in the slide demonstrates two areas of intracerebral hemorrhage in the right lentiform nucleus.
Each year, more than 795,000 people in the United States have a stroke, and it is the fifth leading cause of death in the United States.[16,17] Although low-to-moderate alcohol use is associated with a reduced risk of stroke, heavy alcohol use (chronic or irregular) significantly increases the risk of both ischemic and hemorrhagic stroke.[18,19] Alcohol also has an anticoagulant effect, which is partly responsible for the increased risk of hemorrhagic stroke at higher levels of alcohol consumption.
Alcohol Abuse: Complications and Consequences
Pancreatitis
Alcohol abuse is the second most common cause of acute pancreatitis, after gallstones.[20] However, moderate alcohol use is protective against all forms of pancreatitis.[21] Pancreatitis may develop from an isolated episode of binge drinking or from habitual abuse. Injury to the pancreatic acinar cells creates an inflammatory cascade, leading to pancreatic damage.
Symptoms of acute pancreatitis include dull abdominal pain that gradually becomes more severe, nausea, vomiting, and diarrhea.[22]
Classic physical examination findings of acute pancreatitis include the Cullen sign (edema and bruising in the periumbilical subcutaneous fatty tissue) and the Grey-Turner sign (shown), which is discoloration of the flanks from retroperitoneal hemorrhage. The most serious complications are pancreatic necrosis, pseudocyst, and infection of inflammatory fluid collections.
Alcohol Abuse: Complications and Consequences
The CT scan in the slide demonstrates extensive calcification of the pancreas (red arrow) and a large pancreatic pseudocyst (black arrow).
In chronic pancreatitis, progressive pancreatic damage results in impaired exocrine and endocrine function. The main symptom is pain, but the exact mechanism behind the pain is poorly understood, and there are multiple neurobiologic theories.[23] Pseudocyst formation is the most common complication and may lead to intestinal obstruction, abscess, pseudoaneurysm, or fistula. The 10-year mortality in patients with chronic pancreatitis is 30%.[24] Alcoholism is associated with 70% of cases of chronic pancreatitis, and the incidence of chronic pancreatitis is rising throughout the world.[25]
Alcohol Abuse: Complications and Consequences
Pancreatic Cancer
A 70-year-old man with a longstanding history of alcohol abuse presents with painless jaundice, malaise, and weight loss. A CT scan of the abdomen reveals a mass in the head of the pancreas (red arrow), presumably representing a pancreatic adenocarcinoma. The patient asks if the cancer is treatable.
Which of the following is the most important factor influencing this patient's survival?
- Degree of pancreatic dilation
- Invasion of the superior mesenteric vein
- Invasion of the celiac artery
- Age
Alcohol Abuse: Complications and Consequences
Answer: C. Invasion of the celiac artery.
The endoscopic US image demonstrates a pancreatic carcinoma (mass) obstructing the common bile duct (CBD) but not invading the portal vein (PV) or superior mesenteric vein (SMV). Pancreatic cancer is a frequently occult malignancy that is diagnosed in an advanced stage in half of patients. Chronic inflammation is a major predisposing factor, and patients with chronic pancreatitis from alcohol abuse have a higher incidence of pancreatic cancer and an earlier age of onset.[26] The classic presentation is painless jaundice from a pancreatic head mass.
Surgical excision offers the best chance of cure, but recurrence is very common.[27] Newer surgical techniques may allow resection of the superior mesenteric or portal veins, but involvement of the arterial system is an absolute contraindication for surgical treatment. The 5-year survival rate is only 11.5%. Pancreatic cancer is responsible for 3.2% of all new cancer cases and 8.2% of all cancer deaths in the United States, according to the SEER (Surveillance, Epidemiology, and End Results) Program.[28]
Alcohol Abuse: Complications and Consequences
Cardiac Disease
Although low-to-moderate alcohol intake can provide cardiovascular protection, high alcohol use for an extended period can cause hypertension, coronary artery disease, stroke, peripheral artery disease, and cardiomyopathy, among other conditions.[29,30] Alcohol's toxic effects directly weaken the heart muscle; alcohol also increases blood pressure, oxidative stress, and the risk of thrombosis, while negatively impacting the conductive system (resulting in arrhythmias).[17]
The classic manifestation of chronic alcohol use is heart failure from dilated cardiomyopathy. Dilated cardiomyopathy is an irreversible process in which the ventricular-wall thickness remains normal but the ventricular chambers become enlarged, giving the appearance of thinned walls (shown). Patients have subsequent systolic dysfunction and are at risk for arrhythmias, thromboembolism, and sudden death.
Holiday heart syndrome refers to the development of rhythm disturbances after alcohol use in patients without structural heart disease.[31] Atrial fibrillation is the most common disturbance, and most cases are self-limiting.
Alcohol Abuse: Complications and Consequences
Brugada syndrome, a genetic disorder with an autosomal dominant inheritance, is a cardiac channelopathy that increases risk for sudden death.[32] Electrocardiographic (ECG) tracings in these patients reveal an incomplete right bundle-branch block with one of three patterns of ST elevation in the anterior precordial leads (shown).
Alcohol can unmask or exacerbate Brugada syndrome,[33] triggering ventricular tachyarrhythmias that may lead to syncope, cardiac arrest, or sudden cardiac death. Brugada syndrome is thought to be responsible for 4-12% of all sudden cardiac deaths and 20% of sudden deaths in patients with structurally normal hearts.[34]
Alcohol Abuse: Complications and Consequences
Fetal Alcohol Syndrome
A 35-year-old woman presents to the clinic with her husband after discovering she is pregnant. She does not know when her last menstrual period was, but US confirms a gestational sac (blue arrow) with yolk sac (red arrow). The triage nurse determines that the patient has been drinking alcohol, sometimes to excess. The patient and her husband are concerned about complications to the pregnancy. They are advised that maternal alcohol consumption can be associated with fetal alcohol syndrome (FAS).
During which period of pregnancy does maternal alcohol consumption pose an especially high risk of FAS?
- First trimester
- Second trimester
- Third trimester
- Post dates (post term)
- None of the above; the effect is equivalent throughout pregnancy
Alcohol Abuse: Complications and Consequences
Answer: A. First trimester.
FAS is caused by maternal consumption of alcohol during pregnancy, especially in the first trimester. This can occur when the woman consumes alcohol not knowing she is pregnant. Alcohol moves unimpeded between the fetal and maternal bloodstreams. The incidence of FAS in some parts of the United States has been estimated to be 0.2-1.5 cases per 1000 live births, though prevalence estimates vary among studies.[35] The lifetime cost for one individual with FAS in 2002 was estimated to be $2 million.[35]
A formal diagnosis is made on the basis of characteristic craniofacial anomalies, growth restriction, and central nervous system involvement, including cognitive impairment, learning disabilities, and behavioral abnormalities. A smooth philtrum, a thin upper lip, and short palpebral fissures are typical features; midface hypoplasia, microphthalmia, strabismus, and ptosis may also occur but are less common. FAS is associated with mental retardation and seizures.[35]
Alcohol Abuse: Complications and Consequences
Neurologic Disorders
The coronal brain scans of a 60-year-old man with alcoholism in the slide demonstrate thinning of the corpus callosum and enlargement of the ventricles (on MRI), as well as reduced delineation of the white matter tracts (on diffusion tensor imaging).
Alcohol-related brain damage is caused by direct neurotoxic effects as well as the alcohol metabolite acetaldehyde. Alcohol abuse–associated thiamine deficiency, cerebrovascular disease, hepatic encephalopathy, and head trauma can also result in brain damage.[36]
Delirium tremens is a severe form of alcohol withdrawal that can occur in chronic alcohol abuse. When alcohol use ceases, the loss of inhibitory regulation of excitatory neurotransmitters and neuroreceptors can lead to tremors, diaphoresis, tachycardia, anxiety, delirium, and seizures.[37]
Thiamine deficiency in chronic alcohol abusers can lead to Wernicke encephalopathy, which is characterized by ataxia, ophthalmoplegia, and confusion. Another neurologic complication, Korsakoff syndrome, which often follows Wernicke encephalopathy, involves anterograde and retrograde amnesia, frequently accompanied by confabulation.[38]
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