POTD: Rabies Part 1

Rabies Vaccination

Hey all,

I’m mostly going to be doing POTD’s on topics I’ve accumulated throughout the year that I wanted to look into but never actually did. So, prepare for quite a few fast track complaints (unless I get a request for a topic – just e-mail/text me!).

Anyways, let’s talk about rabies. I’m sure everyone has heard or experienced a great rabies case in their career. No? That’s because since 1980 there has only been about 2-3 reported cases a year in the US, with ~30% of them related to US travelers returning abroad. It is an almost universally fatal disease if contracted but is also 100% preventable if an exposure is identified and given the proper prophylaxis.

So…briefly about rabies…

Epidemiology

-       Estimates 59,000 deaths worldwide, mostly due to inadequate control of rabies in domesticated animals

-       Transmission usually through exposure from saliva from an animal bite

o   No history of transmission from infected patients to healthcare personnel (though personally I look forward to the coming zombie apocalypse)

-       Normal reservoirs: ?dogs/cats to some extent, mostly bats, foxes, skunks, and raccoons

-       Incubation period: 1-3 months on average, though can occur several years later

Clinical Manifestations

-       Prodromal phase (~1 week): Non-specific low grade fever, chills, myalgias, malaise, fatigue, anorexia, sore throat, nausea, vomiting (COVID is that you?)

-       Clinical rabies: Encephalitic (80%) vs. Paralytic

o   Encephalitic = “classic” rabies

• Fever

•   Hydrophobia

•   Autonomic instability – hyperthermia, lacrimation, hypersalivation

•   Pharyngeal spasms and hyperactivity  stupor, coma, and death

• Agitation, aggression, combativeness

o   Paralytic = Less than 20%

•   Ascending paralysis not unlike Guillain-Barre Syndrome

•   As paralysis ascends, respiratory muscles lose tone and respiratory failure and death occurs

  After learning more about this, it’s possible some of us HAVE seen rabies and it’s never diagnosed…….. (I’ll definitely be putting it in my MDM from now on)

Diagnosis

-       As always, a good history and physical is paramount any of the above symptoms surrounding an animal bite is suggestive of rabies

-       Lab diagnosis – requires multiple samples from saliva, skin, serum, or CSF using multiple modalities (sensitivity of a single test not that high)  likely unimportant in the ED

-       Post-mortem – examining brainstem or other neural tissue directly

Differential – aka all of these are 1000% more likely than rabies

-       ANY OTHER CAUSE OF ENCEPHALITIS (West Nile, herpes, autoimmune, etc.)

-       Tetanus (another very common disease that we see frequently)

Treatment – almost universally ends in death. 29 well-documented cases of survival. Survival usually still causes severe neurological sequelae

-       The treatment is always proper prophylaxis

-       Palliation (not joking)

-       Supportive care/ICU level care and strategies = no good evidence/way above our level of care in the ED.

Hopefully you’ve learned a little more than you already did about rabies (although the key clinical symptom does appear to be hydrophobia). I, for one, will be splashing Mak with a little bit of water every day until he becomes agitated and then send him to the ED to be treated for rabies.

Elevated Lactate & Lactate in Sepsis

Elevated Lactate & Lactate in Sepsis

The most worrisome cause of lactate elevation is an elevated lactate from tissue hypo-perfusion & shock, resulting in decreased oxygen delivery to the cells. However, the differential for lactate elevation is broader than simply “shock states.” 

Patients with liver disease such cirrhotics & alcoholics will have poor lactate clearance and can have an elevated lactate level due to hepatic dysfunction. Medications can also lead to a high lactate level, such as albuterol (and other sympathomimetics), metformin, alcohol, & carbon monoxide poisoning (inability to deliver oxygen to tissues). Lastly, muscle activity in heavy exercise and seizures will also result in an elevated lactate level.  

In patients with suspected sepsis, why do we get an initial lactate and repeat it in 6 hours? 

There is an established link between mortality and elevated lactate. This is also a core quality measure decided by the Center of Medicare and Medicaid Services that should be met in patients presenting in sepsis. This is based off of SEP-1, which is controversial and has more or less protocoled sepsis care. The bottom line is CMS wants this measure completed and they hold the purse strings. 

What does the 2021 Surviving Sepsis Campaign say about lactate?

“For adults suspected of having sepsis, we suggest measuring blood lactate. Weak recommendation, low-quality evidence ”

“For adults with sepsis or septic shock, we suggest guiding resuscitation to decrease serum lactate in patients with elevated lactate level, over not using serum lactate. 

During acute resuscitation, serum lactate level should be interpreted considering the clinical context and other causes of elevated lactate

Weak recommendation, low-quality evidence”

The latest surviving sepsis guidelines do recommend measuring lactate levels and guiding resuscitation to decrease serum lactate over not using serum lactate. The panel does recognize that normal serum lactate levels are not achievable in all patients with septic shock, but many studies support resuscitative strategies that decrease lactate toward normal. Serum lactate level should be interpreted within the clinical context and other causes of elevated lactate should be considered. Also, lactate alone is neither sensitive nor specific enough to rule-in or rule-out sepsis. 

In summary, remember we are concerned an elevated lactate may be due to a shock state, such as sepsis. The differential though is broader than shock/hypotension. Lactate can be useful in both diagnosing and guiding resuscitation in sepsis/septic shock, but its use is nuanced and should be interpreted in the wider clinical setting. Remember to get an initial and repeat lactate in suspected sepsis to fulfill the core quality measures set by CMS.

Sources:

Evans, L., Rhodes, A., Alhazzani, W. et al. Surviving sepsis campaign: international guidelines for management of sepsis and septic shock 2021. Intensive Care Med 47, 1181–1247 (2021). https://doi.org/10.1007/s00134-021-06506-y
https://emcrit.org/pulmcrit/acep-septic-shock/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3975915/
Moving Beyond the Centers for Medicare and Medicaid Services' "Severe Sepsis and Septic Shock Early Management Bundle" Core Quality Measure, Jeremy Faust, annals of emergency medicine

POTD: Decubitus Ulcers in the ED

Here's a deep dive into decubitus ulcers, and more specifically the scope of the ED in staging, recognizing when you should be worried about infection, and management tips.

Background: Decubitus ulcers are soft tissue injuries formed from prolonged pressure on the skin. For the decubitus (or lying down) patient, the points under most prolonged pressure involve the tissue between any bony prominence and the patient's bed. Common places we see decubitus ulcers, depending on the patient's position, are shown in the pic below:

Pathophysiology: Multifactorial with a combination of internal and external factors. But the end pathway is always ischemia and necrosis of tissue.

Internal risk factors: Anything that decreases blood flow to pressure sites, promotes inactivity, or decreases sensation are risk factors for decubitus injury. This includes vascular disease, DM, neurological injury, surgical patients, malnutrition. It just so happens that most of these are present in the elderly, and explains why they are the most at risk for decubitus ulcers. Specifically with neurological injury: pressure ulcers are oftentimes very painful. If the patient has decreased sensation, they may not feel the discomfort caused by the increased pressure, and may not readjust to relieve pressure.

External risk factors: Constant external pressure exceeds capillary pressure supplying blood flow to and from tissue. Ischemic tissue eventually becomes necrotic and progresses to pressure injury. Hard static mattresses, physical objects left under patients, and side railings all exacerbate the amount of pressure on vulnerable tissue. Wet tissue from bodily fluids, as well as friction between skin and clothing/bedding also encourage skin breakdown and worsening of pressure injury.

Some evidence suggests that as little as 2 hours of immobility can lead to tissue breakdown from pressure injury.

Staging: 1-4

Stage 1: Skin is INTACT, usually with nonblanchable erythema.

Stage 2: Exposed dermis; partial thickness loss of skin. Erythematous and moist.

Stage 3: Exposed fat. Full thickness loss of skin. Ulceration and granulation tissue likely to be present. 

Stage 4: Exposed fascia, muscle, or bone. Erosion may form tracts deeper than what is initially visible. 

Unstageable: Full thickness skin loss, but depth is unstageable because of existence of eschar or sloughed tissue. If unstageable ulcer is present, there is at least a stage 3 or 4 pressure injury. If the eschar is stable, defined as dry, intact, and no obvious signs of overt infection, then management is to leave it alone with no plans for debridement.

When to Suspect Infection:

At baseline, pressure ulcers are colonized with low levels of polymicrobial bacteria, consisting of skin, urine, and fecal flora. Infection, at least when we refer to an "infected ulcer,"occurs when this bacteria spreads to surrounding, healthier tissue. Infection usually starts with local surround cellulitis and then progresses to involve deeper soft tissue infection, osteomyelitis, and sepsis. Therefore, the extent of an infected ulcer may not be all apparent on physical exam and a high clinical suspicion is needed. Findings include surrounding erythema or discoloration, warmth, fluctuance, exudate, and frank necrosis.

If decubitus ulcer is suspected as the reason for your patient's sepsis, urgent debridement is necessary. In the meantime, start the patient with your normal sepsis cocktail including fluid and antibiotics. Obtain blood cultures for disseminated infection, as well as ESR and CRP if worried about osteo. Choice of antibiotics depends on extent of suspected infection; for mild cellulitis, oral therapy is indicated, but when they arrive to the ED with overwhelming infection, big guns with IV vancomycin and zosyn is a good place to start.

Imaging is not always needed. If diagnostic scans are needed, CT can be a good initial test, but MRI may be needed to measure extent of necrotic tissue.

As far as identifying pathogens in the wound, swab cultures are limited in the information they provide as the infection is often deeper. In this case, a biopsy of the deepest tissue associated with the wound obtained during debridement is the most helpful for goal oriented treatment.

Hope you enjoyed all the fun pictures!

Stay well, friends;

-SD

Sources:

https://www.ncbi.nlm.nih.gov/books/NBK553107/

https://www.uptodate.com/contents/clinical-staging-and-management-of-pressure-induced-skin-and-soft-tissue-injury?search=sacral%20decubitus%20ulcer&source=search_result&selectedTitle=1~150&usage_type=default&display_rank=1#H21

https://www.uptodate.com/contents/infectious-complications-of-pressure-induced-skin-and-soft-tissue-injury

https://reference.medscape.com/slideshow/classifying-pressure-injuries-6005748#38

https://www.shutterstock.com/image-photo/pressure-injury-stageiv-pressuresore-bedridden-medical-1221772201