Alcohol Related Ketoacidosis (AKA)

Alcoholic ketoacidosis is often associated with acute cessation of alcohol consumption after long term consumption. Few cases have been described in binge drinkers as well. It shows up as a high anion gap metabolic acidosis (HAGMA) on blood gas and is typically associated with nausea, vomiting, and GI complaints. Metabolism of alcohol combined with poor glycogen reserves results in elevated ketoacid levels. Death can occur from excessive ketonemia and thus treatment is focused on fluid and electrolytes management. βHB is the pre- dominant ketone product formed in AKA. 

Clinical Presentation

Classically presents with history of heavy drinking followed by vomiting and an acute decrease in alcohol consumption. Common symptoms are nausea, vomiting, and nonspecific abdominal pain. AKA can present with concomitant gastritis or pancreatitis, hypoglycemia, alcohol-withdrawal seizures, GI Bleed, Hepatitis, Sepsis or unrecognized head injury. 


Diagnosis (AKA is a diagnosis of exclusion)

• Low, normal, or slightly elevated serum glucose 
• Binge drinking ending in nausea, vomiting, and decreased intake 
• High anion gap metabolic acidosis
• Positive serum ketones
• Wide anion gap metabolic acidosis without alternate explanation

BHB Ketosis

Normally, the ratio of  Beta HB (beta hydroxybutyric acid) to acetoacetate to 1:1 but in alcoholic ketoacidosis, the ratio can go up to 7:1. Ketone production can be further stimulated in malnourished, vomiting patients. The nitroprusside reagent used to measure urine and serum ketones measures acetoacetate, acetone is only weakly reactive and βHB is not detected at all. Therefore, initial ketone levels may be low or negative in AKA. Mild lactic acidosis may be present due to a shift to pyruvate metabolism toward lactate

In AKA, the average ratio of beta hydroxybutyric acid to acetoacetic acid (5:1) tends to be higher than that which occurs in diabetic ketoacidosis (3:1). With initial therapy, ketone formation shifts toward the production of acetoacetic acid. Thus measured ketone levels rise with initial treatment, although β-OH levels decrease.

   

Differential Diagnosis

• Lactic Acidosis
• Toxic Alcohol Ingestion
• Sepsis
• DKA
• Renal Failure 
• Alcohol Withdrawal 

Treatment

• Dextrose Normal Saline is the initial fluid of choice (to correct hypoglycaemia and acidosis)
• Supplement Electrolytes (Mg, K
• Supplement Multivitamins  (Pabrinex)

• Acidosis usually settles with fluids and bicarbonate use is recommended if pH remains <7.0 despite fluid resuscitation 

Indications for admission

• Persisting Acidosis despite fluid resuscitation
• Unable to tolerate orally
• Other concerning concomitant diagnosis (GI Bleed, Sepsis, Pancreatitis etc)

Take Home

• AKA is diagnosis of exclusion. Rule out other causes of HAGMA (MUDPILES)
• Treatment is focused on Fluid and electrolyte management 

  
References:

1. McGuire, LC, Cruickshank AM, Munro PT: Alcoholic ketoacidosis. Emerg Med J 23: 417, 2006.
   
2. Wrenn KD, Slovis CM, Minion GE, Rutkowski R: The syndrome of alcoholic ketoaci- dosis. Am J Med 91: 119, 1991.
3. Iten PX, Meier M: Beta-hydroxybutyric acid: An indicator for an alcoholic ketoacidosis as cause of death in deceased alcohol abusers. J Forens Sci 45: 624, 2000.
   
   
   Posted by:
   
   
   
   

   

                 

        Lakshay Chanana

        

        Speciality Doctor

        Northwick Park Hospital

        Department of Emergency Medicine

        England

   
   

        @EMDidactic

   
   

Vertigo, “Answers” by EM Lyceum

1. What elements of history do you find most reliable in differentiating central from peripheral vertigo?

Dizziness is the cause of over 10 million ambulatory care visits per year, 25% of which are seen in emergency departments around the US (Newmann-Toker, 2008).  Vertigo is a subset of dizziness in which patients have a false sense of spinning or movement in either themselves or their environment.  The causes of vertigo are numerous, yet are most often categorized as being either of peripheral or central etiology.  Peripheral etiologies include benign diagnoses such as benign paroxysmal positional vertigo (BPPV), vestibular neuritis/labrynthitis, Meniere’s disease, as well as more serious diagnoses such as herpes zoster oticus, and aminoglycoside toxicity.  Central etiologies, however, often include more dangerous pathologies such as brainstem ischemia, cerebellar infarction/hemorrhage, and vertebral artery dissection. Central causes may also include slightly less emergent diagnoses such as migrainous vertigo, multiple sclerosis and Chiari malformations.   The challenge for the ED physician has always been to differentiate the dangerous central causes from the benign peripheral etiologies using history and physical exam, as diseases in both categories often present with vertigo as a major symptom.

On history, the most amount of helpful information can be gleaned from teasing out the timing/duration of the vertiginous episodes.  Although this information may not differentiate central versus peripheral, as lots of overlap exists, it can help narrow the differential diagnosis.  In patients presenting with an acute, prolongedepisode of severe vertigo (i.e., acute vestibular syndrome) the two primary pathologies to consider are vestibular neuritis and cerebellar stroke.  In patients with recurrent, positional vertigo one should consider BPPV as well as Chiari malformation, cerebellar tumors, and multiple sclerosis.  In patients with recurrent, non-positional vertigo,  Meniere’s disease and posterior circulation TIA belong on the differential.

It is a misconception that vertigo that is worsened by head/body movement (including Dix-Hallpike maneuver) is the result of a peripheral cause such as BPPV.  However, the exacerbation of symptoms with head movements have been reported in all causes of vertigo (Kubo, 1988).  Others experts argue that patients with dizziness from ANY cause will feel worse with certain position changes (Kerber, 2009).  Therefore, the characteristic that distinguishes BPPV is not simply an exacerbation of vertigo by head movement, but rather, vertigo that is triggered by positional changes, lasts less than one minute, and then returns to normal between attacks (Kerber, 2009).

Another piece of helpful history is the presence of otic symptoms (hearing loss, tinnitus, ear fullness, etc.), which strongly suggests peripheral etiology (Newmann-Toker, 2007).  Some newer evidence, however, does demonstrate that infarctions of the posterior circulation in the distribution of the anterior inferior cerebellar artery (the blood supply to the inner ear), may rarely cause similar otic symptoms (Lee, 2009).

Other pieces of history that may be helpful include a recent hyper-extension injury ortrauma associated with neck pain and vertigo, which may be indicative of a vertebral artery dissection.  Other central nervous system symptoms including diplopia, dysarthria, weakness, truncal ataxia, and sensory loss are often indicative of a central cause.  Patients with significant stroke risk factors (i.e., hypertension, diabetes, atrial fibrillation, smoking, history of vascular disease) may have vertebrobasilar insufficiency as the cause of their vertigo (Kerber, 2006).  Medications such as aminoglycosides may cause peripheral vertigo, whereas phenytoin can result in cerebellar toxicity and associated vertigo.

Components of the history that may not be as helpful include the presence of nausea or vomiting, which can be seen in both peripheral and central vertigo (Baloh, 1998).  There is also no evidence supporting the presence of a concurrent viral syndrome to be indicative of a peripheral ethology.

2.     What elements of physical exam do you find most reliable in differentiating central from peripheral vertigo?

The crux of being able to distinguish central from peripheral vertigo lies largely in the physical examination.  Hard focal neurological signs (i.e., hemiplegia, hemisensory loss, ataxia, dysarthria, ophthalmoplegia, etc.) clearly point to a central etiology, but unfortunately are found in only approximately 50% of patients with posterior strokes (Kattah, 2009).  So how does one go about differentiating between the two types of etiologies in patients who have no hard neurological signs?  As they say, the truth lies in the eyes…

The classic teaching about nystagmus stills holds up quite well as an accurate method of distinguishing central from peripheral vertigo (Baloh, 2003).  Nystagmus of peripheraletiology is generally found to be horizontal in nature and unidirectional (the fast component of the nystagmus always beats in the same direction, regardless of which way you extend the patient’s gaze).  On the contrary, nystagmus of central etiology is often purely torsional or vertical in nature (usually down-beating nystagmus) and is bidirectional (the fast component of the nystagmus changes directions depending on which direction you extend the patient’s gaze).

              Nystagmus, peripheral                                     Nystagmus, central

Type                Horizontal                                                       Pure torsional or vertical

Direction       Unidirectional                                                 Bi-directional

Although these are reliable physical examination tests, a group of researchers at Johns Hopkins University have developed an even simpler and more accurate 3-step bedside ocular physical examination. They posit that it can quickly and accurately differentiate acute vestibular neuritis from a posterior stroke in patients with continuous vertigo (Kattah, 2009).  The series of tests is called the HINTS exam and is comprised of 3 components: Head Impulse testing, bi-directional Nystagmus, and Test of Skew.  In their prospective, cross-sectional study, they performed the HINTS exam at the bedside of 101 patients in an academic hospital stroke center to try and differentiate between those patients with central versus peripheral etiologies of their vertigo.  Later they confirmed their diagnoses using MRI with diffusion-weighted imaging.  They concluded that the presence of either a normal horizontal head impulse test, direction-changing nystagmus in eccentric gaze, OR skew deviation was 100% sensitive and 96% specific for stroke.  With  MRI having a 12% false negative rate within the first 48 hrs of symptom onset, the HINTS exam was purported by this group to be more sensitive than MRI in initial diagnosis of posterior circulation strokes (Kattah, 2009).

For a video demonstrating how to do the HINTS exam please visit the site of Dr. David Newmann-Toker at: http://novel.utah.edu/Newman-Toker/collection.php#

3.     When do you obtain imaging in a patient with vertigo?  Which study do you use and why?

Brain imaging should be obtained in patients when there is concern for a central cause of  vertigo such as a posterior circulation stroke or vertebrobasilar insufficiency.  A non-contrast head CT (NCHCT) is often the first diagnostic study ordered because of its accessibility in most emergency departments.  NCHCT, however, has poor diagnostic utility in diagnosing lesions of the posterior fossa, because of the amount of bone artifact present.  NCHCT has a sensitivity of only about 16% in the diagnosis of acute ischemic posterior stroke (Chalela, 2007).  As a result, NCHCT should never be used to rule out the diagnosis of stroke in a patient with a possible central etiology.  The only situation where NCHCT reliably identifies a central cause of vertigo is in hemorrhagic infarctions of the cerebellum, in which acute blood is usually evident immediately by CT.  Unfortunately, these account for only 4% of central causes of acute vestibular syndrome.

Instead, the test of choice when a central cause of vertigo is suspected is an MRI, as it allows a better view of the posterior fossa.  In contrast to CT, MRI has a sensitivity of about 80% in detecting lesions of the posterior fossa within 24 hours of symptom onset (Tarnutzer, 2011).  The obvious disadvantage of MRI is it’s often not readily available in the emergency department within a short period of time.  If the integrity of the posterior circulation needs to be assessed, an MRA may also be useful in detecting vertebrobasilar stenosis or dissection.  Although MRI is clearly more sensitive than CT in detecting posterior strokes, MRI was found to have a false negative rate of about 12% in the original HINTS study, meaning that it fared worse than the bedside HINTS exam in detecting posterior strokes (Kattah, 2009).

4.     In which, if any, patients do you perform a Dix-Hallpike maneuver?  In which patients do you perform an Epley maneuver? 

The Dix-Hallpike maneuver is done to confirm the diagnosis of BPPV in patients with recurrent, positional vertigo.  It tests for the presence of an otolith in the posterior semi-circular canal (the most common cause of BPPV).   It is important to understand that while doing the Dix-Hallpike maneuver, vertigo may be reproduced in patients with both central and peripheral etiologies.  Therefore, the most important aspect of the test is  evaluation of the nystagmus, not the reproducibility of the vertigo.  In a patient with BPPV, the Dix-Hallpike maneuver should elicit nystagmus after a latency of a few seconds, and the nystagmus should last about 15-25 seconds only (Kerber, 2009).  Any nystagmus that persists longer than this should not be considered to be a result of BPPV, and other possible central causes should be considered.  The Dix-Hallpike maneuver has a sensitivity of about 50-88% in patients with BPPV (Hoffman, 1999).

For a video on how to properly perform the Dix-Hallpike maneuver, visit the website of Dr. David Newman-Toker: http://novel.utah.edu/Newman-Toker/collection.php#

When a patient with suspected BPPV has a positive Dix-Hallpike maneuver, the patient can be taken directly into the Epley maneuver in an attempt to reposition the otolith and treat the BPPV.  The efficacy of the maneuver can be tested by rechecking the Dix-Hallpike test after the Epley maneuver is performed. The nystagmus should no longer be present if the Epley maneuver was successful.  If the Dix-Hallpike test shows continued nystagmus, the Epley maneuver can be repeated.

Von Brevern, et al. demonstrated that, when compared to a sham maneuver, the Epley maneuver was successful in 80% of patients (compared to 10% of patients in the sham group) in relieving symptoms of vertigo and nystagmus at 24 hours after treatment (von Brevern, 2006).  Further studies have also outlined the success of the Epley maneuver, compared to sham maneuvers, as a useful method of acute treatment as well as long-term treatment.

 5.    Bonus question:  Which medications do you use to treat vertigo? 

In the treatment of acute vertigo, medications should be given to treat nausea/vomiting as well as the acute episodes of vertigo.  Nausea and vomiting can be treated  in the emergency department with any number of phenothiazine anti-emetics including ondansetron, metoclopramide, or promethazine, to name a few.  These medications may also acutely decrease the symptoms of vertigo experienced by a patient.  IV fluids should also be given to assist in the repletion of volume lost through multiple vomiting episodes.

In order to acutely and effectively treat the symptoms of vertigo, often caused by abnormalities in the vestibular system, vestibular suppressants may be used.  The two major classes of drugs used for this purpose are antihistamines (i.e., diphenhydramine, meclizine, dimenhydrinate, etc.) and benzodiazepines (i.e., diazepam, clonazepam, etc.).  Both classes of medications are complicated by side-effects of drowsiness, which may not be desirable, especially in elderly patients (often worsening their complaints of “dizziness”).  These medications, useful in the initial days of significant vertigo, should be discouraged in daily use after the first 24-48 hours. They are believed to compromise the brain’s ability to compensate for long-term vestibular dysfunction and may delay recovery (Baloh, 2003).

Of the two classes of drugs, antihistamines are often considered to be first-line therapy for vertigo, as they appear to be less sedating than their benzodiazepine counterparts.  In terms of comparative efficacy in alleviating vertiginous symptoms, very little data exists.  One double-blind randomized study by Marill, et al., looked at 74 patients and compared 2mg IV lorazepam to 50mg IV dimenhydrinate in the symptomatic treatment of vertigo in the emergency department. They demonstrated that patients given dimenhydrinate had an increased ability to ambulate, less drowsiness, and were significantly more likely to be “ready to go home” compared with the lorazepam group at the 2 hour mark after treatment (Marill, 2000).

Originally posted by EM Lyceum. Shared with Permission. 

Check out EM Lyceum- where everything is up for debate . . . 

Overtesting and Misinterpretation - Urine Dip Pearls

Interpreting lab tests requires a considerable amount of knowledge and experience. One such test is urine dipstick which is often done in the ED to look for blood, evidence of infection, ketones etc. Since Emergency Departments across the globe are working under tremendous amount of time constraints, tests are now being done based of chief complaints (abdomen pain panel, pleuritic CP panel, Headache panel etc.) instead of clinical suspicion of a diagnosis. While this reduces the time to reach a conclusion, it makes evaluation and medical decision making very complex for a clinician. 

What are we supposed to do with a result that we never expected and we never wanted that to be sent at the first place? Positive hstroponin in a very low risk patient, positive d-dimer in a 16 year old who was hyperventilating or a positive urine dip for nitrites in an asymptomatic patient.

We know that we are overdiagnosing and over-treating UTIs. Rates of Misdiagnosis of UTI are up to 40%. Therefore, it is imperative to have have a pre-test probability before we order a urine dip or microscopy. And if it is already reported before you have actually seen the patient, be comfortable in disregarding the results if it does fit in the clinical scenario. 

Having a clinical questions can help. Ask yourself these two questions before you order any test (not just Urine Dip):

1.What are you looking for in the test. Is it Nitrites or blood or ketones? 
2. What is going to be your next step if the result is positive or negative?

Putting Urine Dip into a clinical context differentiates a clinician from other healthcare providers. Treating positive urine nitrites for UTI - Anyone can do that! 

But Medicine is not that simple!

Key points while interpreting a urine dip:

1. Bacteriuria does not equal UTI

If you send a culture on asymptomatic bacteriuria, you might get a positive culture but what if your patient never had any symptoms? The answer is - do not bother sending urine for testing in asymptomatic patients and do not treat asymptomatic bacteriuria (exceptions - Rx in pregnancy in those who are undergoing a urologic procedure). UTI is a clinical diagnosis, not a lab diagnosis. Colony counts and cultures are pointless without symptoms or clinical suspicion. 

2. Leucocyte Esterase (LE) is indicative of pyuria not UTI
Here is a list of things than can cause pyuria:

• HIV
• STDs
• Appendicitis
• Urolithiasis
• Malignancy
• Nephritis 
• Dehydration
• Diverticulitis
• Indwelling catheters

Once again, results for LE needs to interpreted with a clinical context. In neutropenic patients, urine WBCs may be artificially low despite an infection

3. Nitrites 

Nitrates in the urine are converted to nitrites in the presence of Gram-negative bacteria such as E.coli. A positive nitrite test is a indirect marker of bacteriuria, not always a marker of infection (unless patient is symptomatic).

Nitrites are not produced by S. saprophyticus, Pseudomonas or enterococci, so a negative nitrites does NOT rule out UTI. Also watch your method of sample collection. Almost universally, urine is collected in a non-sterile fashion and thus interpretation should be always in the clinical context. Presence of Epithelial cells indicate a contaminated sample. 

Negative leukocyte esterase and nitrite negative almost rules out UTI

4. Elderly with Altered Mental State and UTI - Not always!

UTI is this scenario is pretty much a diagnosis of exclusion (Rule out Neuro and GI causes before labelling as UTI). Asymptomatic bacteriuria is extremely common in elderly. Rx them based on the history of symptoms and confirm your diagnose with a catheterised sample. When history is compromised due to cognitive issues - Look for fever, chills, elevated WCC, CRP, previous episodes of UTI to gauge your suspicion. If the look stable (normotensive, not tachycardia, no fever) then it is reasonable to hold Abx and convey this to the in-patient teams. 

5. He smells of urine, so we think it is a UTI

Anyone who is unkempt, not looked after well and urinates in his pants is going to smell bad. Bad smell is not always an indicator of Urine Infection. Do not prematurely close the diagnosis here. Smell can be affected by a number of factors such a your hydration status, concentration of urea, diet. Do a complete history and physical and then come to a conclusion. 

Take Home

• Do not treat asymptomatic bacteriuria
• Hold Abx if they look stable. Liaise with in-patient teams. 
• Negative leukocyte esterase and nitrite negative makes UTI highly unlikely

References:

Schulz L, Hoffman RJ, Pothof J, et al. Top ten myths regarding the diagnosis and treatment of urinary tract infections. J Emerg Med. 2016 Jul; 51(1): 25-30. 


Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic

Ulcerative Colitis - ED Management

Ulcerative colitis (UC) is a chronic inflammatory relapsing and remitting disease of the colon. The etiology is believed to be autoimmune with some genetic component. Peak incidence occurs in the second and third decades of life with characteristic symptom of bloody diarrhoea. The rectum is almost always involved in UC. 

Factors associated with an unfavourable prognosis include higher severity and extent of disease, a short interval between attacks, systemic symptoms, and onset of the disease after 60 years of age.

Clinical Presentation

Crampy abdominal pain, bloody diarrhea, and tenesmus are typical symptoms of UC. The disease is classified as mild, moderate, or severe depending on the clinical manifestations. 

Truelove and Witts criteria

Extra intestinal Manifestations 

Diagnosis

ED diagnosis of ulcerative colitis rests on the following: 
History of abdominal cramps and diarrhea, mucoid stools, stool examination negative for ova and parasites, stool cultures negative for enteric pathogens, and confirmation of diagnosis by colonoscopy.

Treatment

Mild to Moderate attacks
Most of these patients can be treated as outpatients. A combination of oral (2.4 grams/day) and topical mesalamine is used. Topical glucocorticoid enemas or Mesalazine enemas or suppositories (500 milligrams twice a day) are quite effective in distal proctosigmoiditis and have lower systemic side-effect profiles.

If topical therapy is unsuccessful, steroids (40-60md Prednisolone/day) are effective in inducing a remission in the majority of cases. Antidiarrheal agents are generally ineffective and may precipitate toxic megacolon.

Rx of UC based on severity of disease

Severe ulcerative colitis - Treat with IV steroids, fluids, correct electrolyte abnormalities, broad-spectrum antibiotics, melamine. IV cyclosporine (2-4 milligrams/kg per day) or infliximab (5 milligrams/kg) can be effective in fulminant colitis nonresponsive to IV steroids.

Complications

• LGI Bleed (Most Common)
• Toxic Megacolon - The most feared complication of ulcerative colitis is the development of toxic megacolon. TM occurs as a result of extension of the inflammation beyond the submucosa, causing loss of contractility and dilated colon. Dilation of the colon is associated with a worsening of the clinical condition and development of fever and prostration. Patients with Toxic Megacolon appear toxic with distended, tender and tympanic abdomen. They typically present with fever, tachycardia and shock.

Plain radiography of the abdomen demonstrates a long, continuous segment of air-filled colon greater than 6 cm in diameter. Loss of colonic haustra represent bowel wall edema. Occasionally, features of toxic megacolon, such as leukocytosis, anaemia, dyselectrolytemia, hypoalbuminemia and peritonitis, can be masked in the patient taking corticosteroids.  

Antidiarrheal agents, hypokalemia, narcotics, cathartics, pregnancy, enemas, and recent colonoscopy have been implicated as precipitating factors in toxic megacolon. Rx with nasogastric suction, IV steroids, broad-spectrum antibiotics active against coliforms and anaerobes, and IV fluids. Get a surgical consultation ASAP.

• Perforation
• Bowel Obstruction (due to strictures)
• Carcinoma Colon  (Advanced and prolonged disease)
• Perirectal fistulas and abscesses 

Disposition

Fulminant attacks of ulcerative colitis need hospitalization for fluid and electrolyte management and careful observation for the development of complications. Patients with complications such as GI Bleed, toxic megacolon, and bowel perforation should also be admitted. In addition to toxic megacolon, the indications for surgery include colonic perforation, massive lower gastrointestinal bleeding, suspicion of colon cancer, and disease that is refractory to medical therapy (large doses of steroids required to control the disease). 

Patients with mild to moderate disease can be discharged from the ED.  It is crucial to arrange close follow-up with gastroenterologist, and any adjustment in medical therapy should be discussed prior to discharge.

References:

1. https://clinicalgate.com/toxic-megacolon/
2. Oxford Handbook of Clinical Medicine
3. Tintinalli's textbook of EM - 8th Edition
4. http://fromnewtoicu.com/blog/2016/12/28/toxic-megacolon-1

Posted by:

              

     Lakshay Chanana

     

     Speciality Doctor

     Northwick Park Hospital

     Department of Emergency Medicine

     England

     @EMDidactic