All posts by vmcimchiefs

Acid-Base Simplified

Today we discussed an complicated case of acid base disturbances that our house staff breezed through. Simi presented a young man with acute epigastric pain and emesis after copious alcohol ingestion. It looked like a case of alcohol-induced pancreatitis or gastritis, but his metabolic panel threw everyone for a loop.

Capture

Go through the labs on your own and try to find an explain all the acid-base disturbances.

Here is our suggested method for acid-base learning:

  1. Is the patient acidemic or alkalemic ? A.k.a. is their pH above or below 7.4
  2. What is the primary disorder? Is the bicarb or the pCO2 driving the acidemia /alkalemia?
  3. What is the anion gap? Anion Gap = (Na+) – (Cl- + HCO3-). If there is an anion gap present, there is a concurrent anion gap metabolic acidosis. 
  4. Is there another metabolic disorder? In this case, do the delta gap and use it to correct the bicarb. If the corrected Capture

In this case, the patient is alkalemic and the primary disorder is a respiratory alkalosis because the pCO2 is low and the bicarb is normal. Physiologically, the pCO2 is not the main driver of the process, but we pick it as the primary disorder for the sake of our problem solving shchema. The anion gap is 30 in this patient so there is a concurrent anion gap metabolic acidosis. The delta gap is 18 so the corrected bicarb is 43, which is over 30 so there is a concurrent metabolic alkalosis. 

The patient’s disorders were likely multifactorial. Lactate was 10 and urinalysis showed trace ketones so AGMA was likely a result of alcohol-induced lactic acidosis with starvation/alcoholic ketoacidosis. The metabolic alkalosis was likely due to both contraction and excessive vomiting. The respiratory alkalosis was likely due to severe epigastric pain and anxiety from alcohol withdrawal.

Karl Friedrick Von Ludwig’s Angina

Today we discussed a case of deep neck space infection! Our patient was a middle-aged man with diabetes and poor oral hygiene who presented with right facial pain and swelling with stiff neck and trismus after seeing his dentist for a tooth infection.

We commonly see patients complaining of tooth aches or sore throats before diagnosing them with pharyngitis or dental caries, but how can we know when to suspect a deeper infection??

Signs and Symptoms that should make you think of deep neck space infection:

  • Trismus (inability to open the mouth fully)
  • Drooling
  • Muffled voice (“hot potato voice”)
  • Neck swelling or swelling of the floor of the mouth
  • Bulging of the pharyngeal wall, soft palate, or floor of the oropharynx
  • Neck pain or stiffness, torticollis
  • Crepitus
  • Respiratory distress: stridor, tripoding, cyanosis

When evaluating a patient with dental complaints, especially if any signs or symptoms of infection are present, it is VERY important to palpate the floor of the mouth for any tenderness or swelling. Over 70% of Ludwig’s angina cases are due to dental infections (most commonly the molars) and if we do not palpate the floor of the mouth, we may assume symptoms are due solely to dental problems. Ludwig’s angina is an infection of the submandibular space that is rapidly progressive and life threatening.  

On physical exam, you should feel a bilateral, tense edema of the floor of the mouth with possible neck swelling and tenderness usually without lymphadenopathy. Buzz words for this condition are “woody” or “brawny” cellulitis, similar to necrotizing fasciitis. Our patient exhibited 1cm trismus, poor dentition with many dental caries, fullness and tenderness to palpation in the floor of the mouth, as well as neck tenderness and swelling.

Initial evaluation should include rapid and thorough assessment of respiratory status, including asking about respiratory distress at night because these patients often occlude their airway when laying down. Some cases of Ludwig’s angina do not require intubation and can be managed with IV antibiotics and close monitoring in the ICU. However, any signs of respiratory distress should prompt immediate intubation as this can progress rapidly to airway occlusion. Fibreoptic nasotracheal intubation is preferred, often awake and upright, due to the risk of laryngospasm with oral intubation. Whenever intubating a patient with Ludwig’s angina, all preparations for a possible surgical airway should be made in advance due to the often difficult nature of these intubations. Anesthesia and ENT should be consulted emergently whenever Ludwig’s angina is suspected. These patients should always be admitted to the intensive care unit. Although controversial, many otolaryngologists recommend IV glucocorticoid use to decrease airway edema in the emergent period.

The condition is usually polymicrobial with a variety of oral flora, but when an agent is identified, Group A strep is most prevalent. Empiric coverage should consist of gram positive, gram negative, and anaerobic coverage. Unasyn is the drug of choice empirically, but if any MRSA risk factors are present, vancomycin should be added. These risk factors include IVDU, diabetes, ESRD on HD, residence in long-term care facility, hospitalization in the past year). If the patient is septic and at risk of rapid deterioration, MRSA coverage should be included regardless of risk factors. Pseudomonal coverage should be added for any immunocompromised patients. 

The diagnosis of Ludwig’s angina is clinical, but imaging (CT with contrast) may be performed to rule out abscess and determine the need for surgical drainage. This conditions usually does not include focal purulent collections, but is more typical of an aggressive nonpurulent cellulitis with diffuse infection so surgery is not always indicated.

When extubating these patients, throughout evaluation of airway patency must be performed, often including laryngoscopy prior to extubation and extubating over a guidewire.

Why did Ludwig name it “angina”???

Traditionally, we use angina to describe chest pain of cardiac origin. However, the word comes from the Latin angere and Gree ankhone, which mean choke and strangle. Before the discovery of penicillin, the mortality of Ludwig’s angina was over 50%, many due to asphyxiation.

Thyrotoxic Periodic Paralysis

Yesterday we discussed a classic case of thyrotoxic periodic paralysis…. with a twist. Our patient was a young male of Asian descent with a history of Grave’s disease who fasted for routine lab tests, then ate a high carbohydrate meal, and developed acute lower extremity weakness. His presentation illustrates a classic case of the disease:

Capture

However, his case was slightly atypical because he recently underwent a radioiodine ablation to treat his Grave’s disease and his free T4 and T3 levels were actually normal. Cases of TPP have been reported after radioiodine ablation, thought to be due to a transient hyperthyroid state after ablation. An oral glucocorticoid taper prescribed to decrease chance of worsening Grave’s ophthalmopathy after ablation may have also contributed to his development of TPP.

Treatment consists of potassium replacement. A regimen of 30mEq PO KCl Q2h until improvement begins with a max dose of 90mEq in 24h. This regimen may seem cautious as many of these patients present with potassium levels of less than 2, but they are prone to potassium over-correction so cautious repletion is wise.

The Clots That Traveled Far and Distal

Today we discussed a case of an elderly gentleman who presented for AKI 5 weeks after a FEVAR with bilateral renal artery stent placement for a 6.5cm juxtarenal AAA.

We first reviewed the major risk factors for AAA:

  • elderly age, male
  • smokers
  • connective tissue disease

We then reviewed the USPSTF recommendation for AAA screening, which is one-time screening of all male patients 65-75 with any smoking history

We discussed indications for AAA repair

  • Ruptured -> emergent repair (endovascular management is a possibility)
    • Severe pain, hypotension and pulsatile abdominal mass in 50% of patients
    • Often misdiagnosed as renal colic, diverticulitis, GI hemorrhage, ischemic bowel
  • Symptomatic of any size or configuration who do not have a prohibitive surgical risk for repair should be urgent AAA repair
    • Abdominal pain, flank pain, limb ischemia, systemic manifestations such as fever or malaise
  • Asymptomatic infrarenal AAA <5.5cm = conservative
  • Asymptomatic AAA >5.5cm OR rapid expansion OR co-existing PAD OR female gender = elective repair
  • Asymptomatic AAA > 5.5cm with life expectancy <2 years, no repair

We then started reviewing the case, and quickly found out that this patient’s prior hospitalization was notable for livedo reticularis, blue toe syndrome and ischemic colitis. His discharge Cr was roughly stable and it was only 3 weeks later that he started having a significant rise in the Cr. His urine revealed no RBCs, a single eosinophil and no casts. A CT abdomen/pelvis without contrast revealed no stent migration or kinks and a renal duplex US revealed patent flow.

Nephrology reviewed all the data and were confident in their diagnosis: renal atheroemboli. Here’s what you need to know:

  • Vast majority will be iatrogenic, so look for a precipitating event such as angiography, lytic therapy or cardiovascular surgery
  • Look for subacute kidney injury (peaking 3-8 weeks after the event) and signs of extrarenal embolization (GI bleeding, focal neurologic deficits, blue toe syndrome, livedo reticularis
  • Eosinophilia, Eosinophiluria and Hypocomplementemia may all suggest atheroemboly
  • No proven effective medical therapy in patients with atheroembolic renal disease and management is supportive as well as considering how to prevent further embolization
  • Prognosis is generally poor, as many will have a stepwise decline in their renal function due to scarring as well as new embolic events and up to 1/3 may require renal replacement therapy

 

2nd Degree Heart Block Dissected

Today we went over the case of an elderly man with episodes of lightheadedness for one month who was found to have 2nd degree AV block on EKG in the ED (with old LBBB as well). Capture

EKG Criteria for AV blocks:

1st degree: PR prolongation (>200msec)

2nd degree Mobitz I: Wenckebach, progressively prolonging PR interval followed by a “dropped beat,” or nonconducted p wave

2nd degree Mobitz II: constantly prolonged PR followed by a “dropped beat,” or nonconducted p wave

3rd degree or complete: complete AV dissociation between p waves and QRS’s

As you move from 1st toward 3rd degree, the block is more clinically severe, more likely to need treatment, and more symptomatic. Anatomically as you move from first to third, the block becomes more distal in the conduction system.

2:1 Second Degree AV Block: Is it Mobitz 1 or Mobitz II?

In the above EKG, we see a 2:1 second degree AV block, which means that every other p wave is conducted. This does not allow us to see the progression of the PR interval. How are we to know if it is prolonging (Mobitz I) or constant (Mobitz II)? There are 4 ways to help answer this question:

  1. Look at the company it keeps. If you see periods of 3:2 in your patient’s telemetry, the 2:1 block you see on your EKG is likely the same type of block as the periods of 3:2.
  2. If the PR is >300msec or the QRS is narrow, your block is more likely to be Mobitz I (higher up the conduction system in origin).
  3. Give atropine! If the AV nodal conduction is enhanced (less frequent nonconducted p waves), your block is likely Mobitz I. If there is no response, your block is likely Mobitz II.
  4. Carotid sinus massage: This increases vagal tone, which will increase the blockade in Mobitz I, but improve conduction in Mobitz II by allowing more time for excitability to return to the bundle of His.

 

THE Dermatologic Emergency: SJS/TEN

On January 29th, our very own PGY-2 Hong Le, presented a case of the most well-known dermatologic emergency for our review: an elderly gentleman recently started on antibiotics for a urinary tract infection presents with a full body painful rash.

SJS and TEN are a spectrum of disease, TEN being more severe and SJS less severe. TEN covers >30% of total body surface area and SJS covers <10%. If between 10 and 30 percent of TBSA is covered by the rash, it is termed SJS/TEN overlap syndrome. A good way to estimate body surface area is to use the area of your hand as an estimate of 1%. 

Capturesure SJS/TEN is provoked by exposure to an inciting drug. Complete lists of drugs with reported association with this condition can be found online, but the most notable categories include allopurinol, antiepileptics, antibacterial sulfas, nevirapine (NNRTI), and NSAIDs ending in “-oxicam.” Patients with HIV have a particularly increased risk of developing SJS/TEN. The typical exposure period before reaction is 4 days to 4 weeks, but risk continued for 8 weeks after treatment with a new drug. 

The classic description and progression of SJS/TEN on physical exam are as follows. First, a flu-like prodrome may occur (malaise, myalgias, arthralgias, and fever) 1-3 days before the onset of rash. When the rash begins, it is extremely painful, ill-defined, coalescing macules with purpuric centers on the face and thorax that spread diffusely and symmetrically. These lesions are typically termed “dusky.” It usually spares the scalp, palms, and soles. Soon vesicles and bullae form and within days, the skin sloughs. Mucosal surfaces are involved in >90% of patients, which may cause symptoms such as photophobia, conjunctival itching/burning, odynophagia, dysuria, and painful defecation. Nikolsky sign is positive in these patients (the skin sloughs when tangential pressure is applied). Other diseases with a positive Nikolsky sign include pemphigus vulgaris and staphylococcal scalded skin syndrome. The “wet newspaper sign” is also classic for SJS/TEN, the shiny and lighter tone of exposed skin after a layer of affected epidermis sloughs off. The SCORTEN score can be used to determine prognosis and severity of the condition. 

Treating SJS/TEN is mainly supportive, including removing the offending agent, IV fluids, wound care, nutrition, and electrolyte repletion, but a multidisciplinary approach is necessary. Consults to dermatology, burn surgery, ophthalmology, OBGYN for a vaginal exam if the patient is female, and possible urology consult for males should occur immediately. High suspicion for infection and low threshold to start antibiotics are also beneficial.

There are multiple adjunctive treatments your dermatology consultants may recommend, but additional research is needed on most of them. Cyclosporine, anti-TNF drugs, steroids, IVIG, and plasmapheresis are a few of them.