Yesterday, we discussed transfusion reactions and went through the difference between TRALI and TACO, which can both cause respiratory distress within 6 hours of a blood transfusion, but are very different entities. Here’s a handy table to help you remember the differences:
Fever DDx (MISO!)
Hypertheremia DDx (NEED!)
In clinical practice, impossible to tell the difference between fever (raising of the body’s set point) and hypertheremia (failure of thermoregulation)
*Sincere thanks to Dr. Julie Lee for correcting a critical error in the table!
Today we discussed a variety of topics, and most excitingly, revealed that our inpatient anti-infective therapy guideline is now published on HHSConnect on the ASP page.
Same disclaimer applies: we have no direct clinical experience dealing with COVID+ patients and information has been taken from a variety of excellent resources as listed in the prior post. We make no claims for originality!
Pathophysiology and Stages of COVID
This is key folks. There seems to be a early viral replication phase, followed by a later dysregulated inflammatory response phase marked by ARDS and a cytokine storm. In the early phase, antiviral therapy may be much more helpful than delayed initiation. Once the late phase has arrived the mainstay of treatment will likely be immune-modulating agents (anti-IL6 agents and steroids..more on this later.
Modes of Transmission of COVID
Yes, you read that correctly. There is evidence that aerosolization does occur and therefore in our hospital, we use a N95/face shield for all PUIs and confirmed patients – a move we strongly believe will improve the safety of our healthcare workers (HCWs)
https://www.nejm.org/doi/full/10.1056/NEJMc2004973
Airway Management Prior to Intubation
Sources:
a. ‘Why Did Outbreaks of Severe Acute Respiratory Syndrome Occur in Some hospital Wards But Not in Others – Yu et al in Clinical Infectious Diseases 2007
b. Risk Factors for SARS Transmission from Patients Requiring Intubation: A Multicentre Investigation in Toronto, Canada – PLOS1 2010
Pharmacological Therapies
That’s all for now, much of what was said will likely change. Thank you all for your incredible dedication to each other and to our patients. You all are heroes and I am so proud of you.
Today, Dr. Hakim is presenting a case of COVID-19 infection. We wanted to take this opportunity to give a general overview of COVID-19 and the available data. Just a quick disclaimer: we have extremely limited clinical experience in the treatment of COVID-19 and the following information is collected from various resources and articles. We anticipate that the details of COVID-19 will continue changing rapidly and the information here may become out of date very quickly.
Epidemiology: Median age is 47, slight male predominance (41.9% are female)
Symptoms and Signs of COVID-19: There are 7-9 large studies documenting signs and symptoms of COVID-19 infection with most data coming from China. The largest study, recently published in NEJM: Clinical Characteristics of Coronavirus Disease 2019 in China- W. Guan, Z. Ni, Yu Hu, et al.
Systemic symptoms: Fever, fatigue, myalgias, anorexia, dizziness, headache
Respiratory symptoms: Dry cough, dyspnea, expectoration, pharyngalgia
GI symptoms: Diarrhea, nausea, vomiting, and abdominal pain
***There is no reliable way to distinguish influenza, other viral respiratory infections, and COVID-19 by symptoms alone.
Incubation Period: median of 4 days, range up to 14 days
Lab Findings: White blood cell counts can vary!! Leukocytosis and leukopenia are reported.
Imaging:
Diagnosis here at SCVMC:
Sensitivity and Specificity of Testing:
Coinfection:
Key Resources for further COVID-19 Information:
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.
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:
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.
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:
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.
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:
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.
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:
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
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:
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). 
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:
On February 5th, we went over a fascinating case of a middle-aged man with foot osteomyelitis due to chronic diabetic foot ulcer who presented with back pain, fever, and leukocytosis, found to have epidural abscess.
Below is the illness script for epidural abscess:
SCVMC IM Chief Resident Blog 