March Abstracts

• Ogawa, A., et al, Circ J 70:1372, November 2006: Japanese study looking at pro-BNP in suspected ACS w/o CHF. They compared it to traditional cardiac markers. pro-BNP was much higher in NSTEMI vs STEMI pts. Poorly constructed study w/ lots of data mining. Nothing here should change your management.
  
• LeMay, M.R., et al, Am J Emerg Med 8(6):401, November 2006: Pre-hospital EKG interpretation of EMT's in Ottawa w/ theoretical administration of thrombolytics. They would have overtreated some cases and only saved 44 minutes on average. Since we prefer PCI, nothing here will alter much.
  
• Bradley, E.H., et al, N Engl J Med 355(22):2308, November 30, 2006: Yale study looking at door-to-balloon time. Average time across the nation was 100 minutes. You can improve your steps by having a single page operator, cath staff required to be present by 20 minutes, an in-house cardiologist, the ED doc can call the cath team in and real-time feedback to the ED.
  
• Chung, T., et al, Am Heart J 152:949, November 2006: They examined the utility of BNP in the ED for patients w/ dyspnea. BNP testing was worse in pts w/ a h/o of CHF vs. those w/ a new history. Again, my personal approach is history, physical exam, CXR and the clinical picture will provide all the info you need for whether it's CHF. I don't order this test anymore.
  
• Bursi, F., et al, JAMA 296(18):2209, November 8, 2006: Systolic vs. diastolic dysfunction in pts w/ CHF. Diastolic failure will have decent EF but poor filling of the chambers due to wall resistance. They performed an echo and almost 1/2 of pts w/ CHF didn't have systolic dysfunction (greater than 50%). BNP was mean of 380 in systolic and 183 in diastolic failure. 6 month mortality was 16% for both groups.
  
• Busch, M., et al, Acta Anaesthesiol Scand 50:1277, 2006: Induced therapeutic hypothermia for out-of-hospital cardiac arrest who got a spontaneous return of circulation. Small group (N: 27), cooled to 33 degrees for 12 hours. Slightly more than half survived (but no mention of neuro outcome). Median time to receive target temp was 7.5 hours.
  
• Blaivas, M., et al, J Emerg Med 31(4):407, November 2006: At the Medical College of Georgia, they taught nurses how to use an U/S to enable IV access for difficult pts for obtaining an IV. They had 89% of success rate utilizing the SonoSite. Something we may want to look at (Evan...)
• Humm, A.M., et al, J Neurol Neurosurg Psych 77(11):1267, November 2006: Carotid sinus hypersensitivity as a cause of syncope. Defined by asystole greater than 3 secs and/or drop in SBP by 50. This is a technically difficult dx to make. Only 1 in 40 of pts b/w 40-60 had a positive test. Over 80 yrs old, 40% had it (but did it cause the syncope?). Either way, it's not worthwhile to make it a routine test to determine whether it caused the syncope.
• Baden, E.Y., et al, Can J Emerg Med 8(6):393, November 2006: IV dexamethasone prior to discharge for ED pts w/ benign H/A. They've been treated and are ready to go home. Treated w/ either placebo or Decadron 10 mg IV. 58% of pts w/ placebo still had a H/A as follow-up but only 10% of Decadron pts still had a headache. Something to consider to help prevent bounceback.
  
• Earnshaw, S.R., et al, Stroke 37:2751, November 2006: Use of NovoSeven for the treatment of ICH. This is expensive stuff $10,000 for the large dose, $5000 for medium dose, $2500 for small dose. The most cost-effective dose was w/ the middle dose (80 mcg/kg). I'm still not sold on this medicine, but you'll be hearing more and more for different uses (trauma, etc).
• Cooper, J., et al, Ann Emerg Med 48(4):459, October 2006: Clinical risk for assessing self-harm. Prior history of attempt, prior psych dx, current psych dx, or current use of benzo during this episode all are positive risk factors for completing suicide w/in 6 months. All 22 pts who completed suicide had one of these criteria.
  
• Hennerici, M.G., et al, Lancet 368:1871, November 25, 2006: Placebo or Ancrod for pts w/ ischemic stroke. Ancrod is taken from pit vipers and helps decrease thrombus formation. Ancrod wasn't better than tPA, but coincidentally has performed better than tPA when you review results b/w different studies. Nothing new to take here.
  
• Meurer, L.N., et al, Ann Fam Med 4(5):410, September/October 2006:
  
• Earnshaw, S.R., et al, Stroke 37:2751, November 2006: Medical College of Wisconsin study that looked at all pts who had some sort of medical injury due to trx, error, etc. However when corrected for baseline mortality risk, the magnitude of error is much lower than previously stated.
  
• Rossignol, J.F., et al, Aliment Pharm Ther 24(10):1423, November 2006: Use of Nitazoxanide for treatment of gastroenteritis. It shortens the course by one day. Nothing that we'd really use here or change treatment.
• Bartlett, J.G., Ann Intern Med 145(10):758, November 21, 2006: C-diff is now the most common cause of diarrhea in the US (when identified). More virulent strains and complications now then in prior years. PPI's increase the risk. Fluoroquinolones and cephalosporins are the most common Abx that cause it.
• Springhart, W.P., et al, J Endourol 20(10):713, October 2006: There was no difference in pts w/ renal colic b/w those who received no IVF or those who got large boluses. Interesting of note.
• Turrentine, M.A., Obstet Gyn 107(2, Part 1):310, February 2006: Pts who were on Coumadin and took a one time dose of Diflucan had a 1/3 elevation of their INR. Only 6 patients and no significant bleed.
  
• Shapiro, N., et al, Ann Emerg Med 48(5):583, November 2006: Patients with end-organ dysfunction do worse. However pts w/ SIRS didn't do worse. The bottom line is if you have shock, you're going to do worse.
  
• Micek, S.T., et al, Crit Care Med 34(11):2707, November 2006: Before and after study of utilizing septic shock order sets in a hospital based on the Surviving Sepsis Campaign. 30 vs. 48% mortality and 3 days shorter time in the hospital. May simply be due to more aggressive IVF and early/appropriate Abx. Sponsored by the company that makes Xigris.
  
• Tamir, E., et al, J Emerg Med 31(4):403, November 2006: For patients who are ambulating after MVC, do you need T/L/S spine xrays? No pts out of 1100 had a significant finding. Poor study, but probably not unrealistic.
• Dalton, J.D., et al, Ann Emerg Med 48(5):615, November 2006: Randomized trial for adults w/ ankle sprains to Tylenol vs. Ibuprofen. There was no difference b/w the two groups.
  
• Friedman, B.W., et al, J Emerg Med 31(4):365, November 2006: No change in pts receiving IM dose of corticosteroids for non-radicular LBP.
  
• Tindall, A., et al, Emerg Med J 23:883, November 2006: Skin-wrinkle test for nerve injury in pediatric or non-cooperative pts. W/ autonomic nerve injury, they won't have wrinkles on their hand after wet. Nothing I'd use in the ED.
• Bisset, L., et al, Br Med J 333:939, November 2006: Treatment of lateral epicondylitis (tennis elbow). Steroids work early but the effects change quickly and ultimately doesn't help.
• Walsh, K.E., et al, Pediatrics 118(5):1872, November 2006: After implementation of computer order entry systems in pediatrics, 20% of errors were due to the computer system. Many studies show that they systems have lots of associated risks w/ them and while they may help w/ efficiency to a degree, there are lots of unintended consequences.
  
• Psaty, B.M., et al, JAMA 295(23):2787, June 21, 2006: When doctors are involved in "seeding studies" (studies never meant to be published, but gain acceptance on formulary, pay the doc, get them to prescribe drugs, etc), not only do the docs involved, but their partners end up prescribing whatever pharmaceutical is involved.
  
• Boyd, J.J., et al, Acta Anaesthesiol Scand 50(10):1266, November 2006: For heroin OD's who received pre-hospital narcan and signed out AMA, they had no adverse effects. If they're going to need narcan, they'll need it in the first hour. They state that if you follow a heroin OD for at least one hour and they do fine, they're safe for d/c.
  
• Salo, D., et al, J Emerg Med 31(4):371, November 2006: RCT of continuous Alb SVN vs continuous Alb SVN + Atrovent for the trx of acute asthma. Adding atrovent really doesn't change anything in acute asthma (more beneficial in COPD). They were using 15 mg of Albuterol as part of the continuous trx.
  
• Tsai, W.K., et al, Am J Emerg Med 24(7):795, November 2006: Pig-tail vs large-caliber chest tubes for spontaneous PTX. Use of the pig-tails is just as well and didn't cause significant problems down the line.
  
• Cohen-Kerem, R., et al, Clin Ped 45:828, November 2006: OTC cold remedies for peds pts hasn't shown to be of benefit, but family docs love giving it and pediatricians as well (but not so much).
  
• Turkcuer, I., et al, Am J Emerg Med 24(7):763, November 2006: Turkish study showing U/S is better than x-rays at finding wood or rubber FB in soft tissues. Since we have a SonoSite and 24 hr U/S, better to use that than the needless x-ray for non-metallic FB's.
  
• Ott, M., et al, J Trauma 61(3):607, September 2006: Guess what, trauma pts get lots of radiation (probably more than we should). Try to be judicious when ordering x-rays, CT's, etc.
  

That's it...

A Little Goofy

I found this case when reviewing my "interesting" case files. It has some interesting learning points...

CC: AMS
HPI: 23 yo M who has been progressively altered, ataxic and dropping objects the last 24 hours. + h/o OCD, depression, bipolar and anxiety d/o. Per his father (historian) he'll usually binge drink on a twice weekly basis in order to "curb" his OCD. Just yesterday he was arrested for a DUI. The patient has had some increasing stress as well due to an illness w/ his girlfriend. Per the father he takes Haldol, Klonopin, Depakote, Seroquel and Effexor. The patient is quite somnolent and is unable to provide a history. He'll open his eyes, mumble an incoherent response to the question or repeat the question itself and go back to sleep.

PMHx: OCD, depression, bipolar d/o, anxiety
Meds: Haldol, Klonopin, Depakote, Seroquel, Effexor
SHx: Binge EtOH abuse
ROS: Unable to obtain secondary to AMS

V/S: BP: 141/90 HR: 94 RR: 18 Temp: 99.6 Sats: 96% (RA)

PE: (pertinent findings)

Gen: Somnolent, but arousable. Will try to follow commands but just falls back asleep.

Neck: No meningismus; Negative Brudzinski's and Kernig's

Neuro: No focal CN deficits. MOE x 4, but not coordinated

Diagnostic Testing:

EKG: NSR @ rate of 94; no ectopy; nl QRS, QTc

WBC: 10.6 U/A: neg except for trace ketones

K+: 3.4 Cl: 97 BUN/Cr: 9/0.4 Glucose: 92

Tylenol: neg ASA: neg EtOH: neg UDS: neg

Depakote: 344 Ammonia: 143

Discussion:

Based on this patient's med list and the ataxic, uncoordinated like movements he had, I had a suspicion that he might be a depakote toxicity. Hence besides checking the depakote level, I had a ammonia level drawn. Ammonia can be elevated in patients with depakote toxicity and can contribute to the encephalopathy. Obviously Klonopin, Seroquel, Haldol, EtOH and drugs of abuse can also present with this picture. Given his EtOH abuse history and recent DUI that'd be something to consider, but he had no EtOH odor to him or quite honestly look like he was "just drunk".

After the depakote and ammonia levels came back, I discussed the case w/ toxicology and we started the patient on L-carnitine at 50 mg/kg IV over 5 minutes. A dose was repeated in five hours and a repeat depakote level was ordered in 4 hours. The patient was admitted to the ICU. Later his ammonia levels peaked at 233 and

Valproic acid toxicity:

Valproic acid elevated CNS GABA concentrations. It also prolongs the recovery of inactivated Na+ channels. Oral absorption is rapid (often within 1-4 hours), with peak plasma levels within 3-5 hours. At levels of 80 ug/mL 90% is protein bound, however, in the case of toxicity there is an increase in "free drug" causing a proportional increase in available drug after protein saturation. Elimination is based on first-order kinetics w/ a half-life of 7-15 hours. Therapeutic levels are b/w 50-100.

Valproic acid (depakote) can cause hepatic failure with days or up to two years after first use. Toxicity often results in AMS, lethargy, N/V, and ataxia. LFT's and ammonia levels can be elevated. AMS can be directly related to the elevated CNS GABA levels (like EtOH) or ammonia levels. Patients may have depressed DTR's and pinpoint pupils (mimicking opioids).

Treatment of valproic acid toxicity follows the usual tox guidelines of supportive care. Since it closely mimics opioids, give a test dose of Narcan is reasonable (as well as checking glucose, etc). Since absorption is rapid, charcoal is probably only efficacious if given in the first sixty minutes. Hemodialysis does decrease serum levels (remember it's protein bound) and can be used.

In this particular patient L-carnitine was administered. This treatment has been looked at by some jackasses named LoVecchio and Samaddar (L-carnitine was safely administered in the setting of valproate toxicity. LoVecchio F - Am J Emerg Med - 01-MAY-2005; 23(3): 321-2) and proven to be safe. I'll rip the study later on all its "flaws" but for now we'll accept the gospel according to Frank.

So if you have any interesting tox cases or Frank et al want to comment on this, fire away...

Herky Jerky

From the case files of one of our colleagues...

CC: Seizure

HPI: 24 yo male presents s/p first-time seizure. Per his mother, she went to go pick him up for work. When he didn't answer, she broke down the door and found him actively seizing. He has no history of seizures. He had a traumatic MVC a year before. He has since recovered and been living w/ roomates. The only other history is that he's been coughing for the past few days.

PMHx: Traumatic MVC

Meds: Lexapro, Ativan

SHx: Lives with roomates

ROS: Unable to obtain

V/S: BP: 149/65 HR: 61 RR: 24 Temp: 97.9 (rectal) Sats: 97%

PE: (pertinent findings)

Patient is actively seizing with eyes deviated to the right. + Right facial twitching. No other pertinent findings on PE

Hospital Course:

The patient was given Ativan 2 mg IV to stop the seizures. Later he had mild spontaneous movement of his RUE/RLE. His LUE was "restless" and pulling at items. A CT scan was done using ketamine and the patient was loaded w/ cerebryx.

Labs:

WBC: 49.1 H/H: 17/51 BUN/Cr: 19/2.2 K: 2.8 CO2: 17

UDS: + THC Ammonia: 108

CT head: possible SDH in right posterior falx

CXR: possible "right-sided infiltrate"

LP was performed using ketamine. Results are as follows:

CSF WBC: 11,300 RBC: 3040 Polys: 85% Monos: 15%

The patient was loaded with Rocephin, Vancomycin and Acyclovir and transferred for neurosurgical evaluation.

Discussion:

This patient appeared to have had bacterial meningitis which resulted in seizures and altered mental status. Their CSF later grew out Strep pneumoniae. A couple of teaching points can be taken from this case.

A nice job by the doc involved to get the LP done in a difficult patient . Meningitis has to be considered in any patient with new seizures and/or mental status changes.

From an educational standpoint, perhaps ketamine isn't an ideal choice in this patient due to its side effects of increased ICP. Perhaps this patient had a traumatic GLF and suffered a epidural or SDH and hence the seizures. Propofol might be a better choice (especially w/ the lack of history or witnesses in what precipitated the seizures). Either way, avoid ketamine in patients who have or might have a traumatic brain injury. Also since radiology is calling a "possible" SDH, it would be wise to avoid anything that can bump up the ICP (especially when they're already seizing and probably causing a pretty good spike in their ICP already).

Also remember to give both your pediatric and adult patients a dose of steroids in suspected meningitis. They have been shown to decrease both adverse neurological events and mortality. Dexamethasone is the preferred agent and if you're going to LP, you can give a dose before you even put a needle in their back. Tis better to shoot first and ask questions later (as the departed Hunter S. Thompson would most assuredly agree with). Most regimens involve Dexamethasone 10 mg IV q 6 hours x 4 days ("Steroids in adults with acute bacterial meningitis: a systematic review": van de Beek D - Lancet Infect Dis - 01-MAR-2004; 4(3): 139-43.)

Another question that often arises is who can you LP without doing a CT to r/o space-occupying lesions? General rule of thumbs are that it's safe to LP prior to CT if they fulfil the following criteria: a) do not have new-onset seizures b) immunocompromised state c) signs that are suspicious for space-occupying lesions (papilloedema, focal neural signs) and d) moderate-to-severe impairment of consciousness. If they do not have any of these criteria, then you can safely LP the patient without head CT.

Also remember to give Ceftriaxone 2 g IV for suspected cases and consider the need for Vancomycin +/- Acyclovir as well.

Just a Quick Tug

Here's another interesting case straight from the "classic" board questions series (that actually occur in real life)...

CC: H/A and speech change
HPI: 27 yo F presents w/ a headache and speech change. She had gone to her chiropractor earlier in the morning to get "adjusted". She felt fine afterwards and went home. Later she was at her OB's office when she began to have a H/A. After the appointment she went home and noticed that she had some aphasia and right-sided vision loss. All symptoms have since resolved and denies any current neuro deficits.
PMHx: Denies
Meds: Lexapro, HCTZ
SHx: Denies
PSHx: Denies

V/S: BP: 127/81 HR: 70 RR: 20 Temp: 98.3 Sats: 98% (RA)
PE: (Pertinent findings)
A&Ox4; Visual fields intact; No focal neuro defictis. Unremarkable exam

Initial Diagnositc Testing: Basic labs and beta HCG were negative. CT head was also negative.

Based on this history and symptoms, what would be of primary concern and what would you order?

A CT angiogram of the head and neck were ordered to r/o carotid artery. The patient did end up having a dissection of the proximal left ICA. She had patent intracranial vessels and intact posterior circulation. She was transferred to St. Joe's neurosurgical service for evaluation.

Discussion:
Although uncommon, cerebral artery dissection is an known adverse outcome of chiropractic manipulation. It can also occur spontaneously, after whiplash, neck-stretching, and in certain connective-tissue disorders (Ehlers-Danlos syndrome, Marfan syndrome, etc). It most commonly occurs in the extracranial carotid artery between C2 and the base of the skull.

Symptoms may include transient retinal ischemia, cerebral infarct, face and/or neck pain, Horner's syndrome, audible bruits and a pulsatile tinnitus.

Diagnostic imaging includes CTA or MRA to r/o dissection. Remember that CTA has a 1% complication risk.

Treatment includes neurosurgical evaluation. Heparin will sometimes be started to prevent thrombemboli, but I'd discuss it w/ your consultant before starting treatment.

So go out there and crack those necks...

Pain in the Belly

Another case of mine that involves a relatively uncommon but significant diagnosis...

CC: Abdominal pain
HPI: 2 yo male presents w/ three day h/o abdominal pain. Patient has had an unremarkable PMHx, but for the last three days has had intermittent episodes of abdominal pain. Per parents he's been very fussy and irritable. He'll be fine and then seems to go over to the corner, get on fours "like a dog" and cry and grab his belly. Nothing seems to precipitate these events, they last for a couple minutes and then resolve on their own. He was seen in an UC three days earlier and had x-rays performed that were "negative". Parents were instructed that if symptoms persist, they should come to the ED.

He has no prior surgical history and still have normal BM's. Parents deny fevers, nausea/vomiting, travel, recent Abx use, GI hx, excessive weight loss, trauma, etc. No family h/o pyloric stenosis, but per parents, the UC doc informed them that if symptoms persist, then he should get an U/S. When the pain comes on he seems to grab at his epigastric/periumbilical region. Stools at the U/C were negative for fecal leuks, but parents admit to "foul-smelling" flatus.

PMHx: GERD as infant (no further trx)
Meds: Deny
SHx: Lives w/ parents and one sib
ROS: Negative except for HPI

V/S: HR: 79 RR: 22 Temp: 99.6 Sats: 98% (RA)
PE: (pertinent findings)
Gen: Non-toxic, but fussy and irritable.
Abd: Soft and NT, no obvious HSM. During the exam, he curled up and cried excessively w/ a tense, hard abdomen

Comments: This is a pretty classic presentation for what he ultimately was found to have. Two year old w/ intermittent episodes of crampy, inconsolable abdominal pain has to make you consider this diagnosis and order a specific test that can be both diagnostic and therapeutic...

In the mean time labs had been ordered and were relatively unremarkable.

Labs: WBC: 10.7 Polys: 44% Bands: 3%
Electrolytes, urine all unremarkable

So late on a Saturday night (when he presented), I bugged one of our dear radiologists to come in and perform a barium enema (their choice- the newer literature shows that air enema's can work just as well) to r/o intussusception.

If you've never seen a BE study performed, they can be painfully boring until you get to the end of it (as in this one). For the first 50 minutes, the general excitement was getting the patient adequately sedated enough to tolerate the test and lay still. But once the ileocecal junction was getting closed, the diagnosis was made. There it was found that the contrast would not pass and even more importantly, the bowel was not reducing. It appeared as if he had suffered from an non-reducible intussusception.

The patient was quickly transferred to PCH for surgical evaluation.

So let's review some of the key features of intussusception...

Remember, that it involves any part of the GI tract telescoping into another segment. It's the most common cause of bowel obstruction in children from 3 months - 5 years. Over 60% of the cases are diagnosed in the first year of life. There is a male:female predominance of 4:1.

There is a seasonal incidence after the viral season. Other causes include a Meckel's diverticulum, polyp, HSP, tumors or FB's. Ileocolic intussusception are the most common (as was the case in this child).

As the upper part of the bowel enters into the lower part, it brings along the mesentery. This causes venous engorgement. Later on bowel edema, bleeding and sloughing can produce the classic "currant-jelly stools". However, this is a late-finding and if found the patient is already extremely sick.

The classic story is a child from 6-18 months old who will be fine and then suddenly drop or ball up and be inconsolable. Vomiting is usually rare. If you're lucky, you might feel a "sausage-shaped mass" in the right quadrant during an attack, but again, these children are usually so inconsolable, that I wouldn't rely on this finding.

I've made this diagnosis probably 3 or 4 times in my career and every time it's strictly based on history. The examination is difficult at best. Imagine if your bowel was incarcerated as a two year old. Would you lay back and allow some doctor w/ cold hands to push on your belly? Hence, this is one of those diagnoses where history is extremely important. Usually the parents provide all the info. The story is pretty classic and if they're giving you this type of story, I will refuse to send the child home until some sort of definitive testing is done. These are not the type of cases you can send home and chalk it up to "colic" or a "virus". Just like in this child, if it was allowed to persist, he could of ended up w/ dead bowel and even worse. Therefore, like meningitis, if you consider the diagnosis, you probably have to do the test to rule it out.

With regards to diagnosis, our radiologists still prefer BE's. Air enemas have shown to be just as effective in diagnosis, less radiation and with better rates of successful reduction. Do not perform an enema on a patient with signs of peritonitis, perforation or hypovolemic shock. These patients should obviously go straight to the OR. Ileo-ileo intussusceptions are much more difficult to diagnose and reduce.

All patients who have had a successful reduction should be admitted for observation. Recurrence happens in 0.5-15% of patients. Even after laparatomy, recurrence rate can be 2-5%.

If you have any questions or comments let me know.

Case Reports

Here's an interesting little case that I saw recently....

CC: Alcohol withdrawal

HPI: 54 yo WF presents w/ EtOH w/drawal. Last drink was 48 hours prior. + H/o w/drawal and a possible Sz in the past (unsure if due to DT's). Did later admit to having just a "swig" of listerine 24 hours PTA. Denies methanol, ethylene glycol, etc. No h/o DM

PMHx: Hypercholesterolemia; EtOH abuse

Meds: Denies

PSHx: Denies

SHx: + EtOH abuse; Denies drug use

FHx: DM

ROS: Pertinent for anxiety

V/S: BP: 149/61 HR: 96 RR: 20 Temp: 97.8 Sats: 96% RA

PE: Pertinent findings- tachy in low 100's, anxious, slightly tremulous; Slight epigastric TTP

Hospital Course:

Obviously EtOH w/drawal is number 1-3 on the DDx. I checked a CBC, CMP, lipase. I gave her some Ativan to prevent full-blown w/drawal, monitors, etc. Here's where it gets a little interesting....

Pertinent Labs:

Glucose: 224

H/H: 10.8/32.3

MCV: 100.5

BUN/Cr: 15/0.9

K: 5.0

Cl: 92

Lipase: 179

Bicarb: 9

AG: 41

So why would this patient, who is not diabetic, have such a large AG and profound acidosis? I asked again about co-ingestants (methanol, ethylene glycol, etc). She again adamantly denied these except for the "swig" of listerine 24 hours before. I went ahead and ordered a couple labs with the thought that she might have an interesting condition that I used to see back at the Copa. What would you order and what do you think this might be?

I ordered an ABG, serum acetone, Beta-hydroxybutyrate, lactate and here are the results...

ABG: pH: 7.158 pCO2: 26 pO2: 95 Bicarb: 8.9 Base Excess: -18.5

Acetone: 3+

B-hydroxybutyrate: 76.2 (normal 0-3)

Methanol: neg

Ethylene Glycol: neg

Lactate: 6.3 (Normal 0-2.2)

So what is the diagnosis?

I diagnosed this patient with Alcoholic ketoacidosis (AKA). In review AKA is due to a decrease in fatty acid oxidation in association with poor PO intake or recurrent emesis. There will be a significant increase in serum ketones, mildly elevated glucose, large gap, mild to moderate increase in lactate and a beta-hydroxybutyrate:lactate ratio of 5:1 to 10:1 (normal is 1:1). In this patient the lactate came back soon, but the BHB is a send-out lab (but w/ a ratio of 12:1 helps confirm the diagnosis).

AKA can be seen in first-time binge drinkers or chronic alcoholics. The general starvation results in a decrease in glycogen and insulin stores w/ an increase in catecholamines, glucagon, growth hormone and cortisol levels. Lipolysis and hepatic ketogenesis is stimulated resulting in ketoacidosis.

Of note, AKA typically happens after an acute DECREASE in EtOH consumption (like this patient). They will often show tachycardia, tachypnea, mild to moderate abdominal pain (as seen in this patient, NV, etc. The initial AG will be 21 but elevate later.

Also interestingly, pH may be normal or even alkalemic early in the course. A contraction metabolic alkalosis secondary to protracted N/V may obscure the acidosis.

You want to make sure you also rule out other causes of a metabolic acidosis (methanol, ethlylene glycol, isopropyl etc).

Treatment is symptomatic. Volume repletion and glucose are mainstays of therapy. Glucose will stimulate insulin production which helps alleviate the lipolysis and ketone formation. Insulin is of no proven benefit. Make sure you also evaluate patients for hypophosphatemia and hypomagnesemia (both often seen in alcoholics). You can give the usual thiamine, folate and MVI as well. The acidosis will usually clear within 24 hours.

Hope this was of some educational benefit. Now have a drink...