Author: Dr. Brendan Morrissey
A 51-year-old man self-presents to your inner city ED one Friday evening; he’s complaining of mild abdominal pain and shortness of breath. A quick scan of his old notes at triage shows a background of Chronic Liver Disease secondary to alcohol. He does not appear in distress and is haemodynamically normal, so is placed in the long line for an empty cubicle.
It’s a busy shift with plenty of badness happening in resus, so a few hours pass before a space is found for him to be assessed. He shuffles in and asks for a gown; unfazed by the long wait and well used to the system. He’s brought an overnight bag.
The history doesn’t add much to his initial triage; he complains of a week of constant generalized abdominal pain and nausea. He feels his abdomen has become more bloated and is pushing up on his lungs, making him lethargic and short of breath on exertion. He denies any change in bowel habit, fevers, cough or chest pain.
His history with the department is extensive. A brief look through he previous presentations reveals frequent presentations over the last 10 years with alcohol-related injuries. Never anything life threatening, but the cumulative effect had been enough to get him in and through an alcohol detox programme (after a few false starts). He has been alcohol-free for 6 years. The last few years had seen him become a regular attender at the gastroenterology OPD, where irreversible damage had met supportive care. In stark contrast to his presenting complaint, the sheer volume of information and investigations from his previous presentations is overwhelming. Where to begin…
Alcohol is the most common drug of abuse in the world. Without it many of us would be out of a job. Australians drink about 9L of pure alcohol per year, and as a nation spends $225,000,000 per year in health costs directly related to alcohol. The broader annual cost to the community from social problems related to alcohol is $7,600,000,000. Acute intoxication is a significant contributor to motor vehicle accidents, domestic violence and self-injury, while chronic abuse and dependence decreases life expectancy by an estimated 10-12 years.(1)
The prevalence of high-risk or dependent drinking in Australia is 5%. That’s one in twenty people with patterns of drinking and behavior that will potentially bring them to the ED. Thus it can be safely assumed that the prevalence of high-risk or dependent drinking in the ED waiting room is significantly higher than one in twenty.
The CAGE questionnaire is a simple tool that can be used to screen for alcohol dependence. It consists of 4 questions:
- Have you ever felt you needed to Cut down on your drinking?
- Have people Annoyed you by criticizing your drinking?
- Have you ever felt Guilty about drinking?
- Have you ever felt you needed a drink first thing in the morning (Eye-opener) to steady your nerves or to get rid of a hangover?
A score of two or more is diagnostic, with a sensitivity of 76% and a specificity of 90%. There are other screening tools available, but the problem is rarely the sensitivity of the test or our ability as a profession to remember four short questions; it is simply that we fail to consider alcohol abuse and dependence as an issue.
We are excellent at recognizing the frequent flyers to the ED – the disheveled and bewildered that haven’t seen sobriety since their last failed attempt at detox – but these represent only the tip of the iceberg in terms of problem drinking in the community. Again, one in twenty people in Australia abuse alcohol. This fact should cross your mind at least once during every patient interview. Recognizing the problem should prompt an attempt to intervene, and a good understanding of your local hospital’s drug & alcohol dependence services is essential.
Pondering Chronic Liver Disease, an ED perspective
A number of scoring systems to measure the severity of cirrhosis exist, such as the Child-Pugh score2 and the MELD score (2). These systems use objective measures (bilirubin, albumin, INR etc.) to grade the severity of the patient’s liver failure. Amongst other things, the scores assist in prognosticating patients; giving estimated surgery survival rates and life expectancies. A basic understanding of these scores is useful to the emergency doctor, but far more important is the ability to recognize acute complications of CLD. The most important of these would be gastrointestinal bleeding, hepatic encephalopathy and spontaneous bacterial peritonitis.
1) Acute Gastrointestinal Bleeding
Acute GI bleeding in the setting of CLD is the scariest type of GI bleeding. It goes far beyond the classic ‘brown pants’ terror ED docs know so well. Beyond even ‘black pants’ terror on occasion, it may land squarely on a ‘hosing red vomit’ terror that will leave no psyche or wall/floor/ceiling unscarred. To prevent a GI disaster becoming a resus room catastrophe, I suggest we should understand it and it’s treatment inside and out.
Upper GI bleeding presenting as haematemesis/malaena can have a number of causes in the alcohol-related CLD patient. Alcohol is of course a risk factor for peptic ulcer disease (PUD) and this is by far the most common cause for upper GI blood loss seen in ED. The coagulopathy associated with CLD can sometimes precipitate prodigious blood loss in this setting, turning coffee-ground vomit and malaena into fresh hematemesis and haematochezia (fresh blood PR). Oesophageal varices brought on by cirrhosis and portal hypertension can present as haematemesis/malaena in this patient group and at times can be confused with bleeding PUD. Mortality from variceal bleeds is far higher than that of PUD, and so a high index of suspicion should be kept for this cause in CLD patients.
- Peptic Ulcer Disease
- Oesophageal Varices
- Erosive Gastritis/Oesophagitis
- Mallory Weiss Tear
- Upper GI Ca.
- Other Source: ENT, Haemoptysis
Signs & Symptoms?
- Haematemesis – “Coffee-Ground” Vomit
- Malaena – massive upper GI bleed may present with fresh blood PR
- Symptomatic Anaemia – Classically: postural lightheadedness, lethargy, dyspnea on exertion BUT:
- Chronic or sub-acute GI blood loss may be have minimal symptoms due to haemodynamic compensation
- End-stage CLD can be associated with a chronic hypotension due to decreased intravascular oncotic pressure and 3rd spacing of fluids
- Medications used in CLD (such as β-blockers) may blunt the tachycardic response
Initial management and resuscitation of course takes precedence over precise diagnosis of the source of upper GI bleeding.
ABCs… (with ‘C’ being the problem here):
- Two large bore (16G +) IVCs
- PRBCs and FFP (in anticipation of coagulopathy)
- IV vitamin K
- Stabilisation of the airway – If the patient is obtunded, early intubation should be considered
If an oesophageal variceal bleed is suspected…
The mortality rate for acute oesophageal variceal bleeds is somewhere between 10-20%, so these patients are in trouble. Vasoactive drugs have been shown to be as effect as early endoscopy and sclerotherapy (3), so get in early with the vasoactive agents if you suspect a bleeding varix to be the source of the problem;
- Somatostatin: 250-500mcg IV bolus, followed by 250-500mcg/hr infusion
- or Octreotide: (synthetic somatostatin analogue): 50mcg bolus, followed by 50mcg/hour infusion
Both of these agents act by relaxing mesenteric vascular smooth muscle, reducing portal venous pressure.
If the vasoactive agent-of-choice isn’t working (or unavailable) and emergent endoscopy is unavailable or simply not an option (i.e. the patient is to unstable to get that far), a Sengstaken-Blakemore tube can be life-saving. This piece of equipment is rarely used and incredibly intimidating. The principle behind this is pretty simple; direct tamponade of the oesophagus to control the bleeding. The insertion, however, can be quite complicated and requires practice. An excellent tutorial on the insertion of a Sengstaken-Blakemore tube can be found here on Dr. Scott Weingart’s always-brilliant EmCrit blog (4):
Antibiotic prophylaxis in patients with cirrhosis and upper GI bleeding improves all-cause mortality (5), so a stat does of IV antibiotics should also be given. Local guidelines should be consulted for best coverage – 1g IV ceftriaxone is a reasonable choice.
2) Spontaneous Bacterial Peritonitis (SBP)
SBP should be suspected in every single patient with CLD and ascites, no matter what their presenting complaint. That may seem like an outrageous statement, and it is, but the statistics behind occult SBP are equally outrageous. The one-year incidence of SBP in patients with ascites is around 30%. Up to 30% of these patients may be asymptomatic at presentation, and the sensitivity of physical examination in detecting SBP is somewhere between 50-90% (6).
Signs and symptoms that may point you toward SBP include:
- Fever (80%)
- Abdominal pain (70%)
- Worsening/unexplained encephalopathy
- Abdominal tenderness
Where to tap?
- Landmarks: the left or right lower quadrant; 2-5cm superior and medial to the anterior superior iliac spine
- Avoid surgical scar marks (possible underlying bowel adhesion to abdominal wall)
- Avoid epigastric arteries; keep > 15cm lateral to the umbilicus
- A pre-procedure bedside ultrasound can assist in finding the ideal spot for diagnostic tap for a number of reasons;
- Confirming presence of ascites
- Assessing for underlying bowel adhesions
- Assessing depth to ascites (i.e. thickness of abdominal wall)
How to do it?
Rather than try to describe the procedure, here’s a great video from Dr. Carlo Oller over at theEDexitvideo of therapeutic ascitic drain insertion:
Minor: haematoma, failure of procedure etc.: 1%
Major: bowel perforation, major haemorrhage: < 0.1%
What am I looking for?
A neutrophil count >250/mm3 has a 93% sensitivity and 94% specificity for SBP. (An absolute WCC of 1000/mm3 or a neutrophil count of 250/mm3 is considered diagnostic of SBP) (6)
Gram stain and cultures are negative in up to 40% of cases; culture sensitivity is increased by the addition of testing via the blood culture bottles.
Treatment for SBP
Antibiotics should cover the common organisms (enterobacteria, s. pneumoniae, anaerobes). Local antibiotic guidelines should be consulted for appropriate treatment, but 2g IV ceftriaxone OD or 2g IV cefotaxime TDS or 3.1g ticarcillin-clavulanic acid Q6H would all be considered reasonable empiric cover.
3) Hepatic Encephalopathy
Hepatic encephalopathy is a clinical diagnosis in the CLD patient that is made up of a spectrum of altered mental status, intellectual impairment and personality changes.
Its pathogenesis is poorly understood, but thought to be due to a build-up of nitrogenous waste products (from protein metabolism) usually metabolized by the liver.
Hepatic encephalopathy is a diagnosis of exclusion and other causes of altered mental status in the CLD patient should always be considered (including hypoglycaemia, hyper-/hypo-natraemia, Wernicke-Korsakoff Syndrome and spontaneous/traumatic subdural haematoma).
It’s severity can be classified as follows:
- General apathy
- Lethargy, drowsiness, asterixis
- Stupor with hyper-reflexia
Chronic encephalopathy stage I or II can be managed as an outpatient, but any sudden deterioration in a patient’s staging should be thoroughly investigated.
Signs and Symptoms?
- Altered mental status
- Sleep disturbance
- Fetor Hepaticus (a sweet, faecal smell to the breath that’s difficult to forget)
- Tremor, bradykinesia, shuffling gait (hyper-ammonaemia)
- Lower extremity weakness, hyper-reflexia (hepatic myelopathy)
To investigate hepatic encephalopathy is to investigate for its underlying cause…
- GI bleeding
- Increased protein intake
- Renal failure
- Infection (including SBP)
- Medications (including benzodiazepines, opiates etc.)
Serum ammonia levels are the classic laboratory abnormality in hepatic encephalopathy. That being said:
False positives may be obtained if blood is drawn while a tourniquet is still applied
The test is resource-consuming; it needs to be placed on ice immediately after being taken and hastily couriered to the laboratory for testing
Results vary depending on arterial versus venous sampling
Variations in levels are unimpressive prognostic markers when compared to basic clinical assessment.
For all of these reasons, I find that I rarely rely on ammonia levels when investigating a patient with suspected hepatic encephalopathy.
Treatment of the underlying cause is of course paramount. Following this, lactulose is the mainstay of treatment – 30ml PO/NG Q4-6H.
Back to the Case…
Our 51 year old is a recovering alcoholic with CLD. His most recent liver OPD (from 6 months prior) tells me that he has Child-Pugh grade B CLD, giving him a one year survival rate of 81%. His most recent gastroscopy makes no mention of oesophageal varices, and he has never had SBP in the past. His medication list includes regular lactulose, spironolactone and thiamine.
His vitals reveal a low-grade temperature (37.8oC) and a mild tachypnea (RR 22), but are otherwise normal (HR 70, BP 110/80, sats: 98% RA, BSL: 5.8mmol/L).
His physical exam reveals large ascites and generalized tenderness throughout the abdomen, but without guarding, rebound or rigidity. Beyond his tachypnea, his respiratory exam is unremarkable. PR reveals a large amount of hard stools. He is alert and orientated and his neurological assessment is negative for asterixis or hyper-reflexia.
Fifteen minutes with the patient has told you a lot; his symptoms are most likely due to an accumulation of ascites and you are concerned that SBP may be a complicating factor.
You establish IV access and send off for all the basics (FBC, U+Es, LFTs, lipase, INR and a VBG) but you know the meat of this case lies with his ascites. After verbally consenting the patient, you perform a quick bedside USS, mark your spot and insert an ascitic drain in the LLQ. A cloudy, straw-coloured fluid fills the drainage bag. You send the fluid for cell count, gram stain, culture and susceptibility.
Safe in the knowledge that the patient is neither overtly septic nor suspected of bleeding varices, you withhold antibiotics until the ascitic fluid cell count returns. Concerned about the patient’s faecal impaction and high risk of developing hepatic encephalopathy, you write him up for suppositories and regular lactulose (30ml Q4H PO).
Baseline bloods show no significant change from previous, importantly his renal function is maintained and his electrolytes are within normal limits. The ascitic fluid cell count returns as follows;
– Leukocytes: 400/mm3
– Neutrophils: 80%
A neutrophil count of 320/mm3 increases your suspicion of SBP enough to commence antibiotics. As the patient has no known allergies, you commence 2G ceftriaxone IV OD. The patient is already feeling better, 3L of ascites has drained and his dyspnea has been relieved. You discuss the patient with the admitting gastroenterology team who, grateful for you excellent management, happily accept the patient under their care. By the time the antibiotics are being hung you are already back in resus facing the next unfolding drama…
- National Health and Medicine Research
- Council, Australian Government. http://www.nhmrc.gov.au/your-health/alcohol-guidelines/alcohol-and-health-australia
- D’Amico G, Pagliaro L, Pietrosi G, Tarantino I Emergency sclerotherapy versus vasoactive drugs for bleeding oesophageal varicose in cirrhotic patients. Cochrane Database of Systematic Reviews. 2010. Available from: http://onlinelibrary.wiley.com/store/10.1002/14651858.CD002233.pub2/asset/CD002233.pdf?v=1&t=i0vpukeo&s=114be7403eddfa215ce6a09fe3ed8107411e2d9b
- Weingart S. EmCrit Blog http://emcrit.org/procedures/blakemore-tube-placement/
- Chavez-Tapia NC, Barrientos-Gutierrez T, Tellez-Avila FI, Soares-Weiser K, Uribe M. Antibiotic prophylaxis for cirrhotic patients with upper gastrointestinal bleeding Cochrane Database of Systematic Reviews. 2010. Available from: http://onlinelibrary.wiley.com/store/10.1002/14651858.CD002907.pub2/asset/CD002907.pdf?v=1&t=i0vpoc9j&s=dc2f64609ff952b0828a442cfed2cdc2ff28cb38
- Tintanelli J. Tintanelli’s Emergency Medicine: A Comprehensive Study Guide 7th Edition. McGraw-Hill; 2010.
- Carlo Oller, theEDexitvideo – https://www.youtube.com/watch?v=6d-L6Hni6A4