Status Epilepticus & Serotonin Syndrome

By vmcimchiefs

Today we talked about the case of a young woman who presented after suicide attempt by ingestion of multiple prescription medications, found to be obtunded, initially in status epilepticus and later with exam findings concerning for serotonin syndrome.

Clinical Pearls

  • Continuous EEG is indicated if a patient is not returning to baseline mentation 15 mins after a seizure to rule out non-convulsive status epilepticus.
  • Status epilepticus is defined as a seizure lasting > 5 mins or > 2 discrete seizures between which there is incomplete recovery of consciousness.
  • Treatment of status epilepticus involves acute management with IV/IM benzos, urgent long-term control with IV fosphenytoin (preferred), phenytoin, or valproic acid.  Remember that keppra is more useful in suppressing future seizures than treating an acute episode.
  • Serotonin syndrome is a clinical diagnosis and manifests with neuromuscular activation like tremors, hyperreflexia, and clonus (generally worse in lower extremities).  Use Hunter’s criteria to help with diagnosis.

Status Epilepticus

  • When is continuous EEG needed?
    • If patient is not returning toward baseline in 15 mins after a seizure, goal is to rule out nonconvulsive seizures
  • How to define status?
    • > 5 mins OR
    • > 2 discrete seizures between which there is incomplete recovery of consciousness
  • Non-convulsive status epilepticus
    • Suspect if LOC not improving by 10 mins after cessation of movement
    • Mental status remains abnormal for 30-60 mins after movement cessation
    • Dx requires a 24-hour EEG (we don’t have one ☹)
    • Treatment is the same as generalized status epilepticus, but prognosis is worse (mortality 65% vs 27%)
  • Treatment of status
    • Assessment and supportive treatment
    • Initial pharmacologic therapy
      • Ativan (2 mg IV q1-2 mins), total dose 0.1mg/kg
        • Watch out for respiratory depression and hypotension
        • Alternatives: versed 0.2mg/kg IM, valium 0.2mg/kg IV
    • Urgent long-term control
      • Fosphenytoin (preferred): 20 mg/kg at 150mg/min
        • Give extra 10 mg/kg if not responding
        • Dephosphorylates into phenytoin.  It’s more soluble in water and less likely to precipitate in the skin and vessels.
      • Phenytoin: 20mg/kg at 50mg/min (slower than fospheny)
        • If infused too fast, can irritate skin/vessels causing skin necrosis
      • Valproic acid: 20mg/kg at 5 mg/kg/min
        • Sometimes the preferred choice in patients with known generalized epilepsy b/c phenytoin can provoke absence seizures in that population.
      • What about Keppra?
        • Technically not FDA approved for status.  It has weak evidence to support its use.  More useful in suppressing subsequent seizures after status has been controlled.

Serotonin syndrome:

  • Clinical diagnosis. Serum serotonin concentrations do not correlate with clinical findings.
  • Severe disease can lead to DIC, rhabdo, renal failure, and ARDS.
  • Diagnostic criteria: use Hunter’s (84% sensitive, 97% specific)Hunter's decision rule
  • DDx
    • NMS
    • Anticholinergic toxicity
    • Malignant hyperthermia
    • Sympathomimetic intoxication
    • Sedative-hypnotic withdrawal
    • Meningitis
    • Encephalitis
  • Serotonin syndrome may be distinguished from other causes of agitated delirium on the basis of neuromuscular findings. Whereas patients with serotonin syndrome show signs of neuromuscular activation (eg, tremor, hyperreflexia and clonus that are greater in the lower extremities, ocular clonus, and increased muscle tone), patients with sympathomimetic toxicity or infections of the central nervous system lack these findings.
  • Treatment
    • Supportive care and sedation
      • Chemical sedation preferred over physical restraint
    • Autonomic instability
      • High BP: esmolol or nitroprusside (Short acting). Avoid longer acting agents
      • Low BP: neo or epi. Avoid idirect agents like dopamine because they are converted to epi and norepi.  When monoamine oxidase is inhibited, epi and norepi production at the cellular level is not controlled and could lead to an exaggerated HD response.
    • Hyperthermia
      • No benefit to Tylenol b/c increase in body temp is due to increased muscular activity rather than alteration in the hypothalamic temperature setpoint.
      • If temp >41.1, then sedate, paralyze, intubate
    • Antidote: cyproheptadine
      • Histamine receptor antagonist. Also has weak anticholinergic activity
      • 12 mg loading dose, then 2 mg q2h until clinical response is seen.
      • Is sedating (good) and can also cause transient hypotension.

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Hyponatremia due to secondary adrenal insufficiency

By vmcimchiefs

Thanks to Jess for presenting the fascinating case of a middle-aged woman with family history of autoimmune disease who presented with acute onset of fatigue and abdominal pain, found to have vitiligo on exam.  Work up revealed hyponatremia due to a secondary adrenal insufficiency, pancytopenia, and panhypopituitarism possibly due to a yet to be diagnosed autoimmune disorder!

Clinical pearls

  • Remember that hyponatremia is a problem of water regulation that can be compounded by low solute intake.
  • Primary adrenal insufficiency is disorder at the level of the adrenal glands and manifests with low sodium and high serum potassium levels.
  • Secondary adrenal insufficiency is disorder at the level of the pituitary and manifests with low/normal sodium and normal potassium levels (because low cortisol leads to high ADH levels and hyponatremia).
    • Make sure to do work up to rule out panhypopituitarism.  Keep in mind that the most sensitive test for HPA access integrity is LH/FSH.
  • Tertiary adrenal insufficiency is disorder at the level of the hypothalamus and presents similarly to secondary AI.
  • Test for adrenal insufficiency with a cort-stim test and/or AM cortisol and ACTH levels.

Hyponatremia

Remember these three steps to working up hyponatremia:

  1. Is there a sodium problem? check serum osm
  2. Are the kidneys responding appropriately? check urine osm
  3. Is ADH revved up for a hemodynamic reason? check urine Na 

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Adrenal insufficiency

Adrenal insufficiency
Source: NIDDK.gov

Primary AI:

  • Failure of adrenal glands
  • Causes: Addison’s (most common in the US), infiltrative processes (TB, sarcoid), hemorrhage, toxins
  • Labs would show ↓Na and ↑potassium (b/c aldosterone is gone)

Secondary AI:

  • Failure of pituitary (low ACTH)
  • Causes: pituitary lesions, surgeries, TBI, drugs
  • Clinically may present with loss of other anterior pituitary hormones
  • Labs would show ↓Na (because low cortisol leads to high ADH levels) but normal potassium levels (b/c aldosterone is active)

Tertiary AI:

  • Failure of hypothalamus (low CRH)
  • Causes: more commonly iatrogenic (cessation of high dose glucocorticoid therapy without taper) or post surgical interventions.

Hypopituitarism

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Hypophysitis:

  • Inflammation of the pituitary
  • Four categories based on histologic findings:
    • Lymphocytic
      • Most common form
      • Seen in late pregnancy and post-partum period
      • Also associated with CTLA4 inhibitors like ipilimumab
    • Granulomatous
      • Idiopathic or secondary to GPA, sarcoid, TB
    • Plasmacytic (IgG4-related)
    • Xanthomatous (most rare)
  • Clinical presentation
    • Headache out of proportion to exam findings
    • Preferential decrease in ACTH and TSH ⇒ adrenal insufficiency and hypothyroidism
  • Prognosis:
    • Pituitary size eventually normalizes but pituitary loss of function is often permanent.

 

Angioedema and hyperkalemia management

By vmcimchiefs

Thanks to Audris for presenting the case of a middle-aged man with vasculopathy on ACEi who presented with angioedema requiring intubation!  We discussed the  diagnostic work up and management of angioedema as well as hyperkalemia!

Clinical Pearls

  • First order of business when suspecting angioedema is the ABCs!
  • Treat angioedema in the acute setting with H1 blockers and steroids, even if you are suspicious of a non-histaminergic pathway.
  • Always assess for concurrent anaphylaxis (hypotension or bronchospasm in addition to hives or angioedema).  If anaphylaxis is present, then treatment involves IM 0.3-0.5 mg of 1:1000 dilution epinephrine (1mg/mL), repeat every 20 minutes until symptoms resolve (max 3 doses)
  • If you have access to a functioning kidney, favor loop diuretics over cation exchange binders (i.e. kayexalate) to lower serum potassium!
  • Patiramer is much better tolerated than kayexalate and has a more favorable side effect profile.
  • Calcium gluconate has a role in the treatment of hyperkalemia when EKG changes are present. Give a dose and repeat the EKG.  If no improvement, repeat to a maximum of 3 doses until EKG has normalized.

Angioedema 

  • 3 pathophysiologic subtypes:
    • Mast cell/histamine mediated
      • Etiologies:
        • Allergic reactions: food/insect stings, latex, drugs. Can also be idiopathic. IgE type 1 hypersensitivity
        • Direct mast cell release: drugs (opiates, contrast). IgE is not involved.
        • ASA/NSAIDs: via IgE or direct mast cell release
        • Chronic urticaria w/w/o angioedema
      • S/sx affecting organ systems other than the skin? Suspicious for anaphylaxis ⇒ give epi
      • Treatment: H1 blockers, glucocorticoids. 
    • Bradykinin mediated
      • Inhibition of enzymes involved in the degradation of bradykinin, or deficiency/dysfunction of complement C1 inh
      • More prolonged time course, develops over 24-46 hours and resolves within 2-4 days
      • Relationship between trigger and onset of symptom is not as apparent
      • Not associated with other s/sx. More common to have abdominal pain due to bowel wall involvement.
      • Treatment: bradykinin pathway mediators (ecallantide, icatibant), C1 inhibitor concentrate, or plasma replacement.
    • Unknown mechanism
      • Idiopathic angioedema
      • Infections (in children)
      • CCBs
      • Other drugs: sirolimus, everolimus, amiodarone, metoprolol, risperidone, paroxetine, and etanercept, inhaled cocaine.
      • Herbal meds
      • Urticarial vasculitis
      • Hypereosinophilic syndrome and Gleich syndrome

 

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Hyperkalemia

Agents that reduce serum potassium via transient intracellular shift:

  • Insulin: give with D50 if normoglycemic to avoid hypoglycemia and be sure to check FSG hourly for 4 hours after to ensure no hypoglycemia develops
  • Albuterol (10-20 mg) nebs: this is significantly higher than the dose we give in COPD (2.5 mg) and is equal to ~8 treatments! So make sure to continue the nebs when the patient arrives on the floor from the ER if they are still hyperkalemic.
  • NaHCO3: best for management of chronic hyperkalemia in the outpatient setting.  In the acute management of hyperkalemia, alkalinization of serum with a large bicarb load can lead to a reduction in serum calcium levels.  Lower serum calcium can lead to more cardiac membrane instability and fatal arrhythmias!

Agents that eliminate potassium from the body:

  • Loop diuretics: first choice if a functioning kidney is available!
  • Cation exchange binders: preferred when kidneys are not available
    • Patiramer (available at VMC), much more tolerable than kayexalate and highly effective at lowering serum potassium.  Like kayexalate, it works over hours to days.
    • Sodium zirconium: similar to patiramer but not currently available
    • Kayexalate: not pleasant to take orally. Also carries with it the slight risk of colonic ischemia especially in post renal transplant patients and those with baseline colonic dysfunction (due to infection or inflammation).
  • Dialysis

Indication for using calcium gluconate: when EKG changes are noted.  Repeat doses (maximum 3) until EKG changes have resolved.

Stroke in a 23 year old… secondary to a neck massage 2/13/2019

By vmcimchiefs

We have a very bizarre case of a 23 year old woman, with a history of hypertension, presenting as a stroke alert. She has dysarthria and focal right-sided deficits, and she required intubation for airway protection. She has no prior stroke or clotting history, no illicit drug use (other than marijuana), and no significant family history. CT of the head was unremarkable, but CTA revealed a… vertebral artery dissection! We later learned that the patient was in the middle of getting a massage when the stroke occurred!

That’s right, this is a case of cervical artery (more specifically the vertebral artery) dissection secondary to traumatic massage!

Stroke typically is due to atherosclerotic disease in most cases, but if you need a case that occurred in a young patient, and you’ve ruled out everything else that would present similar, consider the following:

Stroke in young patients 

  • Coagulopathy
    • APLS (one of the most common)
    • DIC
    • HIT
    • Hypercoagulable/hyperviscosity states
  • Vascular
    • Vasculitis
      • Primary: Takayasu, GCS, Kawasaki, PAN, ANCA
      • Secondary: TB, HIV, syphilis, fungi, SLE
    • Dissection (most common in young patients)
    • Trauma
    • Structural malformation i.e. AVM, aneurysms
    • Cerebral venous sinus thrombosis
  • Metabolic
    • CADASIL
    • MELAS
    • Fabry’s disease
    • Homocysteinuria
  • Drugs
    • Cocaine
    • Meth
  • Cardiac
    • Congenital defects
    • PFO/ASD leading to paraoxysmal stroke
    • Arrhythmias
    • Endocarditis
    • Rheumatic valve disease

Vertebral artery dissection: 

Epidemiology

  • Can occur at any age and usually infrequent, but vertebral arterial dissection in general is a common cause of stroke in the young.
  • Carotid artery dissection is much more common than vertebral.
  • Incidence: 1-1.5 per 100,000.
  • Spontaneous dissections of the carotid and vertebral artery account for ~ 2% of ischemia strokes but in young and middle age patients, they can account up to 10-25%.
  • Peak incidence at 5th decade of life, occurs earlier in F > M
  • Most of these patients likely have underlying connective tissue pathology leading to weakening of artery structural integrity but this is a theory.

Pathophysiology

  • False lumen expansion leading to cerebral ischemia from hypoperfusion or thromboembolism, also can cause neurological sx from compression of adjacent nerves/vessels leading to CN involvement, Horner syndrome, pain, etc.
  • Main mechanism, as revealed by angiography studies, point toward a thromboembolic mechanism from the dissection leading to stroke.
  • Hemorrhage due to rupture, expanding hematoma can also lead to focal neurological signs.

Risk Factors

  • Connective tissue disorders (i.e. Ehlers Danlos, Marfans, ADPKD, osteogenesis imperfecta, subclinical/unnamed)
  • Yoga
  • Migraine
  • Coughing
  • Painting a ceiling
  • Vomiting
  • Sneezing
  • Sudden neck movement
  • Trauma
  • Chiropractic manipulation, estimated 1 in 20000 spinal manipulations lead to a stroke.

Presentation

  • Most cases have a precipitating event
  • Intracranial dissection
    • 50% of cases result in subarachnoid hemorrhage
  • Extracranial dissection
    • Associated with trauma, vertebral artery is most mobile and vulnerable to mechanical injury at C1 to C2 as it leaves the transverse foramen of the axis vertebra and enters the intracranial space.
    • Severe neck pain, dizziness, vertigo, double vision, ataxis, dysarthria are common symptoms.
    • Lateral medullary and cerebellar infarctions are common
    • Typical: Local pain, HA, ipsilateral Horners, CN palsies, hemiparesis typically ipsilateral
    • Exam: Hematoma, vascular bruit (1/3 in carotid dissections, usually absent on vertebral), Horner’s syndrome, neck tenderness

Diagnosis

  • Catheter angiography used to be the gold standard, nowadays moving toward…
  • MRA
  • CTA

Management

  • Anticoagulation for at least 3-6 months to prevent thromboembolic complications unless there is hemorrhagic transformation of the infarct, an intracranial aneurysm, or intracranial extension.
    • Most ischemic damage is actually due to thromboembolic effect, not hypoperfusion.
  • Surgical: May be required for SAH/intracranial VAD or if the defect fails to heal on its own
    • Endovascular stenting used for extracranial carotid or vertebral artery dissection when medical mgx fails, anticoag or thromboiysis does not exclude subsequent endovascular therapy but ideally endovascular intervention should be done within 6 hours.
  • Thrombolytics: Consider in extracranial dissection, contraindicated in intracranial dissections or aorta involvement.

Prognosis

  • Extracranial VAD: Generally has good prognosis, estimated 50% of patients will recover with no neurological deficit and 25% with moderate to severe deficits.
  • Intracranial VAD: Prognosis is generally pretty poor.

Take Home Points:

  • Cervical (Carotid more common than vertebral) artery dissection is a common cause of strokes among young patients.
  • Chiropractic manipulation, even massages, are risk factors for cervical artery dissection!
  • A good portion of patients with cervical artery dissection might have underlying, sometimes subclinical, connective tissue abnormalities.

Lupus Nephritis

By vmcimchiefs

Shout out to Paige for admitting the interesting young woman with no medical history who presented with blurry vision, found to be in hypertensive emergency and nephrotic syndrome.  Her work up revealed diffuse proliferative lupus nephritis (class IV) without any other clinical features of lupus!

Clinical Pearls

  • Proteinuria is primarily caused by three processes: 1) overflow (due to elevated paraprotein levels), 2) glomerular disease, 3) tubular disease (rarely reaches nephrotic range)
  • Renal involvement is noted in ~50% of patients with SLE and can present as nephrotic and/or nephritic syndromes.
  • The most common and severe form is diffuse proliferative lupus nephritis (class IV)
  • Keep in mind that SLE flare is associated with a normal/low WBC, normal/low CRP, and absence of fever.  Infection, which can instigate a lupus nephritis flare, would cause an elevated WBC, elevated CRP, and fever.
  • Lab findings suggestive of SLE flare also include an elevated anti-dsDNA (correlates with disease activity), low complement levels (especially C3), worsening proteinuria, and elevated creatinine.
  • Treatment involves an induction phase with cytoxan or MMF plus solumedrol followed by a maintenance phase with the goal of reducing urine protein excretion to <0.33 g/day.

Hypertension urgency/emergency:

  • Urgency: BP>180/120 without end organ damage
    • Manage with orals, goal to lower (not necessarily correct) over 24-48 hours
  • Emergency: elevated BP + end organ damage (brain, eye, heart, kidney)
    • Manage with IV meds, reduce DBP by 10-15% over the first hour, then by 25% over the next 6-12 hours.
    • Special situations:
      • Lower rapidly in acute aortic dissection (goal SBP <110 ASAP)
      • Recent ischemic stroke: do not lower BP unless > 220/120 (> 185/110 if received reperfusion therapy)

Lupus

  • Female to male prevalence is 9:1
  • Diagnose using Systemic Lupus International Collaborating Clinics (SLICC) criteria.  Must have > 4 (at least 1 clinical and 1 laboratory) OR biopsy proven lupus nephritis with a positive ANA or dsDNA
  • Autoantibodies:
    • dsDNA is 50% sensitive but 97% specific –> can monitor disease activity
    • Smith is 10-20% sensitive but >90% specific
  • Work up of presumed flare:
    • Important to distinguish flare from acute infection but keep in mind that infection can trigger flare
    • SLE flare:
      • Low WBC and normal CRP (except when serositis is present)
      • Fever is unusual
    • Infection:
      • High WBC and high CRP
      • Fever is common 
  • Treatment:
    • Plaquenil for all unless contraindicated
    • Mild/mod:
      • plaquenil, NSAIDs, low dose steroids (pred 5 daily)
    • Severe
      • Acute: high dose steroids
      • Chronic: Immunosuppressive agents (MTX, cyclosporine, cyclophosphamide, azathioprine, mycophenolate, belimumab)
  • Prognosis
    • Worse with pediatric onset, ethnic minority, renal involvement, increased number of diagnostic criteria, low complement, e/o end organ damage
    • High association of CVD and SLE

SLE and renal disease

  • Renal involvement is common and eventually occurs in ~50% of SLE patients
  • 10% progress to ESRD
  • High mortality compared to SLE without nephritis
  • More common and severe in African Americans, Hispanics, Asians
  • Classifications of GN: can evolve from one to another
    • Minimal mesangial lupus nephritis (class I)
      • Earliest and mildest form
      • Rarely diagnosed b/c pts have a normal U/A, no or  minimal proteinuria, and normal Cr
    • Mesangial proliferative lupus nephritis (class II)
      • Microscopic hematuria and/or proteinuria
      • Light microscopy would show mesangial hypercellularity or mesangial matrix expansion
    • Focal lupus nephritis (class III)
      • Hematuria, proteinuria, some HTN, decreased GFR
      • Less than 50% glomeruli affected by light microscopy
      • Segmental glomerulonephritis
        • A: active lesions –> focal proliferative
        • A/C: active and chronic lesions –> focal proliferative and sclerosing
        • C: chronic inactive lesions and scarring –> sclerosing
    • Diffuse lupus nephritis (class IV)
      • Most common and most severe
      • Hematuria, proteinuria, nephrotic syndrome, HTN, reduced GFR
      • Hypocomplementemia (esp C3) and elevated anti-dsDNA during active disease
      • >50% of glomeruli are affected
    • Lupus membranous nephropathy (class V)
      • nephrotic syndrome, Cr normal or slightly elevated
      • Diffuse thickening of the glomerular capillary wall and subepithelial deposits
      • Can present without any other clinical or serologic manifestations of SLE
    • Advanced sclerosing lupus nephritis (class VI)
      • Slow, progressive renal dysfunction with proteinuria and relatively bland urine sediment
      • Global sclerosis >90% of glomeruli
      • Active GN no longer observed
  • Treatment:
    • Best to initiate early
    • Aimed at proliferative lupus nephritis
    • Induction
      • 3 – 12 months: goal is to obtain renal response.
      • Cytoxan or MMF PLUS solumedrol 250-1 g/day x 3 days (former takes 10-14 days to have an effect so the latter is much faster) or prednisone 60 mg/day
    • Maintenance
    • Response:
      • substantial reduction in urine protein excretion to <0.33 g/day
      • improvement or stabilization of serum creatinine
      • improvement of urinary sediment

Approach to glomerular disease:

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* can be nephritic or nephrotic

Chronic Chest Pain and This X-ray… 2/11/2019

By vmcimchiefs

Gray Medicine had an interesting case of a 80yo F with history of treated TB (60 years ago), thoracic artery aneurysm s/p recent TEVAR, presenting with 3-4 months history of throbbing chest and back pain. She was admitted one month prior to the same complaint, CXR and CT Cx did not reveal significant pathology other than mild distal TEVAR graft dilatation. She presents 1 month later with worsening chronic chest pain, anorexia, weight loss.

This is the chest X-ray during this current hospitalization…

Miliary.png

Burn this image into your head! This is a classic miliary pattern on a chest radiograph! The term miliary stems from millet seed, a term used to describe a group of small-seeded species of cereal crops or grains

Miliary2.jpg

Subsequent chest CT revealed innumerable bilateral pulmonary nodules, which were not present a month prior.

NewCTScan.gif

Let’s go through possible causes for a miliary pattern on a chest radiograph. In general it can be divided into three categories. The DDx can be quite wide!

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In our case, given that our patient is an elderly woman with a remote history of treated TB, this presentation is highly concerning for miliary TB leading to reactivation. In general, miliary and disseminated TB are often used interchangeably. Disseminated TB refers to TB that affects at least two organ systems.

The most commonly affects organs are:

  • Lungs
  • Liver/GI
  • Spleen
  • Adrenals
  • CNS

Our patient was placed on airborne, and ultimately her sputum was MTB PCR positive! She has TB!

Presentation of Miliary TB

  • Very common: B-symptoms, FFT, typically subacute to chronic. 80-95% will have a fever.
  • Miliary, unlike typical TB, can present with acute sepsis or respiratory failure.
  • Pain/organ dysfunction based on location of the spread. Basically can affect anywhere. Hepatic TB, 79% of cases are due to miliary TB. Other commonly affected organs are spleen, adrenals, BM, lymphatics, and CNS.
  • Other manifestations: DIC, hyponatremia, pan-cytopenia, 50% cases will have normocytic anemia.

Risk Factors

  • Immunocompromised status
    • HIV
    • Extremes of age (infants, elderly)
    • Immunosuppressives
    • Post transplant
    • Other medical co-morbidities (CKD, cirrhosis, EtOH, etc)

Diagnosis

  • Chest radiograph: Classic faint reticulonodular infiltrate uniformly throughout lungs.
  • CT is more sensitive for miliary TB and usually is recommended. Typical finding might reveal numerous 2-3mm nodules but this is not specific.
  • Tissue, fluid, or lymph node biopsy
  • Gastric aspirate
  • Ultimately combination of clinical diagnosis with support labs/imaging.
  • Gold standard: AFB and culture + MTB PCR
  • All patient should have mycobacterial blood cultures
  • Urine mycobacterial cell wall glycolipid lipoarabinomannan (urine LAM) is a highly specific test with high sensitivity in HIV patients for disseminated TB.

Management

  • Intensive Phase: HREZ (aka RIPE) x 2 months
    • R: Rifampin
    • I: Isoniazid
    • P: Pyrazinamide
    • E: Ethambutol
  • Continuation Phase
    • After, 2 months of HREZ (RIPE), the continuation phase consists of 4 months of isoniazid and Rifampin.
    • Choice of medication and duration will change depending on resistance of the organism and location affected
  • Corticosteroids: Indicated if meninges or pericardium is involved.
  • Make sure to fill out a GOTCH form (not the GOAT form, as someone answered on Kahoot this morning) for Santa Clara County if you have a patient with active TB since a safe dispo will involve multiple disciplines and careful planning!

 

Amaurosis Fugax 2/5/2019

By vmcimchiefs

We presented a case of a 63yo M with 30-pk-yr tobacco use, HTN, HLD, and prior CVD 7 months ago presenting with acute onset vision loss of the left eye, described as “seeing through a black mesh with spots of clear vision.” His symptom lasted for 2 hours before gradually resolving on its own. His cardiovascular and neuro exam were unremarkable, and his fundoscopic exam was normal other some mild AV nicking (a sign found with long standing hypertension). Labs and imaging including CTA did not find any acute etiology. A MR of the orbit was also done without any abnormal findings.

Ultimately pt was diagnosed with transient monocular vision loss (TMVL) most likely secondary to an episode of TIA!

Common things being more common, the most common cause of transient monocular vision loss is ischemia/vascular related!

Ischemic/Vascular Etiology

  • TIA
  • CRVO: Classic painFUL vision loss, flame hemorrhage (blood and thunder descriptor) on fundoscopic exam
    • Acute angle closure glaucoma is the most common factor predisposing to retinal retinal vein occlusion
    • Other risk factors: Sickle cell, HIV, Waldenstrom, sarcoidosis, syphilis
  • CRAO: Classic painLESS vision loss, cherry red spot with retinal pallor is a classic description
  • Carotid artery syndrome (transient retinal hypoperfusion or microemboli)

Neurology Etiology

  • Optic neuritis
  • MS
  • NMO
  • Optic nerve ischemia
  • Increased ICP

Inflammatory Etiology

  • GCA
    • Association with polymyalgia rheumatica
    • Typical patient demographics: Age > 55, F > M (2:1), Scandinavian/Northern European ancestry
    • Other associated sx: Fever, headache, jaw claudication, scalp tenderness
    • ESR and CRP typically elevated but this is NOT always the case!

Other

  • Glaucoma
  • Idiopathic
  • Smart phone use in the dark (I am not kidding), please see this article for more details

Management of TIA

In addition to treating risk factors i.e. HTN, HLD, DM2, a question often came up…

To DAPT or not DAPT?

CHANCE, a multicenter, randomized, placebo-controlled trial published in 2013 (Wang et al.) in the NEJM, revealed that DAPT within 24 hours after a TIA or mild ischemic stroke is beneficial in reducing 90-day stroke risk without an increase in bleeding complications vs aspirin monotherapy. This study was done in China with a patient population with higher incidence of undertreated modifiable risk factors and greater cerebral vascular disease burden, hence its applicability to an American patient population is unclear.

Then the POINT trial came along funded by the NIH, which saw the same benefit in DAPT after TIA/ischemic stroke but with increased bleeding risk compared to aspirin monotherapy.

Bottomline: CHANCE indicates 21 days of DAPT post TIA/ischemic stroke is helpful without increasing bleeding risk, and in POINT, 90 days of DPT is also beneficial but it increases bleeding risk. Per 2018 AHA/ASA guideline:

  • In patients presenting with minor stroke, treatment for 21 days with dual antiplatelet therapy (aspirin and clopidogrel) begun within 24 hours can be beneficial for early secondary stroke prevention for a period of up to 90 days from symptom onset.