POTD: Cavernous sinus thrombosis (CST)

Clinical Scenario:

A 30-year-old woman presents with headache, fever, and decreased vision in her right eye over the past 24 hours. Examination reveals exophthalmos of the right eye and no pupillary reflex and a clear anterior chamber. When asked, she denies weakness and numbness.

What is the most likely diagnosis?


Last week we talked about cerebral venous sinus thrombosis (CVST), today let’s talk about cavernous sinus thrombosis (CST), or the infected subset of cerebral venous sinus thrombosis.

What is it?

  • Cavernous sinus thrombosis (CST) is a rare condition, defined as a septic thrombophlebitis of the cavernous sinus. It is caused by a bacterial infection that typically originates in the face, sinuses, ears, or orbits. Most infectious etiologies in cavernous sinus thrombosis are from Staphylococcus or Streptococcus species. 

  • The two cavernous sinuses are located on both sides of the sella turcica. Important structures are located in, or run through, the cavernous sinus, including the pituitary gland, cranial nerves III, IV, V and VI, and the internal carotid arteries (ICA)

  • It causes significant morbidity and the mortality rate is at 20-30%.

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Risk Factors

  • Sphenoid and ethmoid sinusitis are the most common causes of CST. 

  • Other risk factors include dental infections, facial cutaneous infections, otitis media, maxillofacial surgery, and trauma.

Presentation

  • Most patients will have fever, headache, and vision changes/ocular complaints (proptosis, periorbital edema and/or chemosis). 

  • Most will also have external ophthalmoplegia, due to venous congestion of orbital tissues, extra-ocular muscle inflammation and/or inflammation of cranial nerves III, IV and VI. 

  • Other symptoms include eyelid erythema, autonomic dysfunction, sensory changes in the ophthalmic and maxillary trigeminal nerve distributions, pupillary abnormalities, and papilledema. 

  • Vision loss is rare as the orbital nerve lies outside the cavernous sinus. 

  • CST commonly spreads from one eye to both within 24 to 48 hours.

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Evaluation

Blood cultures, CBC, and coagulation studies (PT and PTT) should be ordered, as well as CT of the head and orbits with contrast.

Treatment

  • Parenteral antibiotic treatment should be started with gram-positive coverage (nafcillin plus a third-generation cephalosporin or vancomycin if concerned for MRSA). The patient should be admitted with neurology and ophthalmology consultations

  • Anticoagulation and steroids, remain controversial.

    • Steroids may confer improved cranial nerve function.

    • Anticoagulation may confer a risk of systemic and intracranial bleeding and may result in dissemination of septic emboli. Consider anticoagulation only if there is no evidence of severe bleeding risk or current hemorrhage.

Differences between CVST and CST

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POTD: Trauma Tuesdays - Concussions

Clinical scenario:

A 16-year-old boy presents after hitting his head in a collision with another player during a soccer game. He denies loss of consciousness but complains of a moderate headache, nausea, and difficulty concentrating. 

Which of the following represents appropriate next steps in management?

A. Admit the patient to the hospital for overnight observation

B. Clear the patient to play after 48 hours if his symptoms resolve

C. Discharge with instructions to get follow-up care and not return to play

D. Order a head CT to rule out the presence of an intracranial bleed or swelling

The correct answer is C. 

Concussions

What is a concussion?

The term "concussion" is often used in the medical literature as a synonym for mild TBI but more specifically describes a pathophysiological state that results in the characteristic symptoms and signs that individuals may experience after a mild TBI. 

Symptoms

Rapid-onset short-lived neurologic function impairment that resolves on its own. These symptoms reflect functional disturbance rather than structural injury.

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Diagnosis

If one or more of the following:

  • Symptoms, including somatic (headache, nausea, off balance), cognitive (“ in a fog,” slow), or emotional (rapidly changing)

  • Physical signs, such as loss of consciousness, amnesia, although LOC is not required

  • Behavior changes, such as irritability

  • Cognitive impairment, such as slowed reaction times

  • Sleep disturbance, such as insomnia

Evaluation

  • Concussion is a clinical diagnosis, and there are a variety of sideline assessment tools (that are outside the scope of the ED) that include measurements of orientation, symptoms, gross cognition, and physical examination findings (e.g. Standardized Assessment of Concussion (SAC)Balance Error Scoring System (BESS), computerized neurocognitive testing, and the Sport Concussion Assessment Tool version 5 (SCAT5 or Child-SCAT5)).

  • Physical exam should include: 

    • assessment of the cervical spine (+/- immobilization with c-collar if cervical spine injury suspected)

    • detailed neurologic assessment (including mental status, cognitive functioning, and gait/balance)

    • structural brain imaging (i.e. CT scan or MRI) if concern for structural injury (e.g. acute brain bleed)

Discharge Precautions

This is arguably the most important part of your role in the concussed patient. Thankfully, the CDC has a ton of great literature on the subject.

Pediatric Care Packets:

  1. Pediatric Discharge Instructions

  2. Symptom-Based Recovery Tips

  3. Pediatric Care Plan

Adult Care Packets:

  1. Adult Concussion Fact Sheet

  2. Adult Concussion Brochure

  3. Adult Care Plan

References:

PEER IX

http://www.emdocs.net/concussion-update/?fbclid=IwAR3KSyGMyb-55DTXUWRkTXRLBurnrvULl2zPhZb4xIyiJH8_idVktsaDTJA

https://www.uptodate.com/contents/acute-mild-traumatic-brain-injury-concussion-in-adults?search=concussion&sectionRank=3&usage_type=default&anchor=H25&source=machineLearning&selectedTitle=1~79&display_rank=1#H25

https://www.cdc.gov/HeadsUp/

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POTD: Alcoholic Ketoacidosis

Today’s topic will be for the people who used this 3-day weekend for a bender:

Alcohol Ketoacidosis (AKA)

Clinical Scenario:

Someone who has been on a bender and shows up to your ED after two days of vomiting, has a low bicarb, elevated anion gap, elevated lactate, urine ketones, and an elevated BHB level...probably has AKA. 

Background

  • Alcoholic ketoacidosis (AKA) is a starvation state in an alcoholic or binge drinker

  • Alcohol + No Food + Dehydration = AKA

  • Most often associated with acute cessation of alcohol consumption after chronic alcohol abuse

  • Can also be associated with first-time alcohol binge

  • one of the causes of anion-gap metabolic acidosis 

Clinical Features

  • episode of heavy drinking followed by vomiting and an acute decrease in alcohol consumption

  • N/V, nonspecific abdominal pain

  • can have associated gastritis or pancreatitis

  • normal mental status, but if patient is altered, look for toxic alcohol ingestion, postictal states from withdrawal seizures, or occult head injury

  • exam with acetone odor on breath

  • tachypnea (Kussmaul respiration), tachycardia, and signs of dehydration

Pathophysiology

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Nicotinamide adenine dinucleotide (NAD, or “Needs Additional Dextrose”) is depleted by ethanol metabolism, leading to inhibition of the Kreb’s cycle (or aerobic metabolism) in favor of ketone formation, depletion of glycogen stores, and suppression of insulin secretion  

Diagnosis

  • low, normal, or slightly elevated glucose

  • binge-drinking that ends in N/V and decreased intake

  • wide AG metabolic acidosis, especially one without an alternative diagnosis

  • (+) serum ketones

  • can have associated hypophosphatemia, hyponatremia, and hypokalemia

Treatment

  • Sugar and water!

  • Glucose stimulates insulin production, which stops lipolysis and halts further ketone formation. Glucose also increases oxidation of NADH to NAD, thereby further stopping ketone production. 

  • Start with 5% dextrose in NS. Once fluid and electrolyte losses are replaced, change fluids to 5% dextrose in 1/2 NS until oral intake is assured.

  • Give 100 mg thiamine (facilitates Krebs cycle)

  • Correct electrolytes

  • Repeat Chem7 to see if bicarb improving. If it’s not, consider ethylene glycol or methanol poisoning. This is the time for fomepizole and a call to your local toxicologist or poison center!

Disposition

Discharge if tolerating PO!

References

https://emcrit.org/toxhound/aka-aka/

https://lifeinthefastlane.com/ccc/alcoholic-ketoacidosis/

Tintanelli’s

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