• Sickle cell disease complications (cerebral ischemia, parvovirus, splenic sequestration, anemia)
• Pediatric hematologic emergencies (hemophilia, vitamin K deficiency)
• Pediatric anemia types

• Block 13 (pp 1119-1125): Zoonotic infections (cutaneous anthrax, zoonoses from pets), and transition to tropical/travel medicine topics
• Block 14 (pp 1126-1136): Tropical infectious diseases - Chikungunya, Relapsing fever, Viral hemorrhagic fevers (Yellow fever, Ebola/Marburg, Crimean-Congo hemorrhagic fever, Lassa fever), Japanese encephalitis, Cysticercosis, Trypanosomiasis, Leishmaniasis

PG Notes & Viva Questions

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SECTION OVERVIEW

• Pages 1119–1125 (Block 13): Zoonotic Skin Infections, Cutaneous Anthrax, Pet-associated Zoonoses
• Pages 1126–1136 (Block 14): Tropical & Travel Medicine - Chikungunya, Relapsing Fever, Viral Hemorrhagic Fevers, Japanese Encephalitis, Cysticercosis, Tropical Parasitic Diseases

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PART 1: DETAILED NOTES

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1. ZOONOTIC SKIN INFECTIONS (pp. 1119–1121)

Key Concept

Major Bacterial Chancriform Zoonoses

Fungal Zoonoses

• Blastomyces dermatitidis - cutaneous blastomycosis
• Sporothrix schenckii - sporotrichosis (dog/cat owners, veterinarians at risk)

Viral Zoonotic Dermatoses

• Vaccinia (cowpox), Paravacinia (pseudocowpox), bovine papular stomatitis
• Occur on hands/forearms of cattle, sheep, goat, horse workers

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2. CUTANEOUS ANTHRAX (pp. 1119–1120)

Epidemiology

• Accounts for 95% of all anthrax infections ("woolsorter's disease")
• Common in livestock workers, agriculture workers
• Recent outbreaks in injection drug users
• Most common sites: hands, fingers; also arms, lower legs, feet

Pathogenesis & Clinical Course

1. Anthrax spores deposited in skin wound
2. Day 1–5: Painless/pruritic macule at inoculation site
3. Macule → ulcerative site with multiple serosanguinous vesicles (vesicles are infectious)
4. Ulcer → painless black eschar → falls off within 2 weeks
5. If purulence present → suspect secondary bacterial superinfection
6. Untreated mortality: 5–20%, with shock possible

Diagnosis

• Gram stain or culture of vesicular fluid

Treatment

• Naturally acquired (not bioterrorism): Penicillin or amoxicillin × 3–7 days
• Bioterrorism concern: Oral ciprofloxacin × 60 days; doxycycline as alternative

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3. ZOONOSES FROM HOUSEHOLD PETS (pp. 1121–1125)

Key Points

• Dogs and cats: majority of zoonotic infections in North America
• Growing trend of backyard poultry → >70 Salmonella outbreaks since 2000
• Small rodents, pet birds, reptiles, aquarium fish: minority of cases
• Hand washing is key to prevention

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4. CHIKUNGUNYA FEVER (p. 1126)

Epidemiology

• Self-limited arboviral infection with epidemic potential
• Vector: Aedes mosquito species (same as dengue, Zika)
• Significant in Caribbean and South America
• Incubation: 1–12 days (usually 2–3 days)

Clinical Features

• Fever, severe myalgias, fatigue, headache
• Morbilliform rash
• Occasional thrombocytopenia
• Hemorrhagic complications are RARE (distinguishes from dengue)
• Long-term arthralgia sequelae are common (chronic polyarthritis)

Diagnosis

• Elevated IgM antibodies in serum or CSF

Treatment

• Supportive only

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5. RELAPSING FEVER (p. 1126)

Etiology

• Borrelia species (NOT B. burgdorferi)
• Transmitted by lice or tick bites
• Rare in travelers; suspect in those with refugee/displaced population contact

Pathogenesis

• Borrelia reproduces in body fluids → endotoxins affecting liver, spleen, capillaries

Clinical Features

• Incubation: 3–10 days
• Fever, chills, headache, myalgias
• Severe cases: ARDS, CNS involvement, liver failure
• Spontaneous abatement then relapse (multiple times - hence "relapsing")

Diagnosis

• Identifying spirochetes in blood peripheral smear, CSF, or bone marrow
• Best sampled during febrile period

Treatment

• Tetracycline, doxycycline, or erythromycin
• Ceftriaxone for CNS involvement

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6. VIRAL HEMORRHAGIC FEVERS (pp. 1127–1131)

Key Concept

Most common cause of acute hemorrhagic fever in temperate climates: Neisseria meningitidis

Transmission Routes

• Infected mosquito/tick bites
• Close contact with rodent/bat excreta
• Direct contact with infected individuals (notably Ebola)
• Onset of fever: within 3 weeks of exposure

Isolation Protocol (CRITICAL for exam)

1. Negative-pressure room isolation
2. High-efficiency particulate-arresting (HEPA) respirators
3. Gloves and gowns
4. Immediately contact public health authorities

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A. YELLOW FEVER (p. 1128)

• Flavivirus; vector: Aedes aegypti mosquito
• Endemic in tropical South America and sub-Saharan Africa
• Incubation: 3–6 days
• Most cases: mild self-limited illness
• Severe cases (15–25%): fever + jaundice + hemorrhage (triad)
• "Faget sign": bradycardia despite high fever (relative bradycardia)
• Liver: eosinophilic degeneration of hepatocytes (Councilman bodies)
• Laboratory: elevated transaminases, bilirubin, PT; leukopenia, thrombocytopenia
• Black vomit (hematemesis) = poor prognosis
• Treatment: supportive
• Vaccine available (live attenuated); required for entry to many endemic countries

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B. EBOLA AND MARBURG VIRUSES (p. 1128)

• Filoviruses (filamentous RNA viruses)
• Natural reservoir: fruit bats
• Transmission: direct contact with blood/body fluids of infected individuals or animals
• Incubation: 2–21 days (Ebola); 5–10 days (Marburg)
• Clinical: fever → myalgias → hemorrhage → multiorgan failure
• Case fatality rate: up to 50–90% in outbreaks
• Diagnosis: RT-PCR; ELISA for antibodies
• Treatment: supportive; experimental antivirals (remdesivir); Atoltivimab/maftivimab/odesivimab (Inmazeb) for Ebola
• Strict contact/droplet isolation mandatory

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C. CRIMEAN-CONGO HEMORRHAGIC FEVER (p. 1129)

• Nairovirus (Bunyaviridae)
• Vector: Hyalomma ticks; also direct contact with infected animal blood
• Endemic in Africa, Balkans, Middle East, Russia, Central Asia
• Incubation: 1–13 days (tick bite) or 1–3 days (contact with blood)
• Phases:
  1. Prehemorrhagic: fever, headache, myalgias, N/V, diarrhea
  2. Hemorrhagic: petechiae, ecchymoses, GI bleeding, epistaxis (days 3–6)
  3. Convalescence: if survived
• Lab: leukopenia, thrombocytopenia, elevated liver enzymes
• Treatment: Ribavirin (IV/oral); supportive care
• Healthcare worker infections documented - strict PPE required

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D. LASSA FEVER (p. 1129)

• Arenavirus
• Reservoir: Mastomys (multimammate) rat
• Endemic in West Africa
• Transmission: contact with rat urine/droppings; person-to-person via body fluids
• Incubation: 6–21 days
• Clinical: 80% subclinical or mild; severe cases: hemorrhage, encephalopathy, deafness
• Sensorineural hearing loss in 25% of survivors (key distinguishing feature)
• Lab: elevated AST is a strong predictor of death (>150 IU/L = poor prognosis)
• Treatment: Ribavirin IV (most effective if given early); supportive
• Mortality: 1–2% overall; up to 15–20% in hospitalized patients

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7. JAPANESE ENCEPHALITIS (p. 1130)

• Leading cause of viral encephalitis in Asia
• Flavivirus; vector: Culex mosquitoes (breed in rice paddies)
• Reservoir: pigs and wading birds
• Incubation: 5–15 days
• Clinical: Most infections (99%) asymptomatic or mild febrile illness
• Symptomatic disease: fever → headache → rapid neurologic deterioration
• Signs: altered consciousness, seizures, focal deficits, Parkinsonian features (rigidity, mask-like facies)
• MRI: bilateral thalamic lesions (characteristic)
• CSF: lymphocytic pleocytosis
• Diagnosis: IgM in CSF or serum
• Treatment: supportive
• Vaccine available (inactivated; recommended for travelers to endemic areas)
• Mortality: 20–30%; survivors: 30–50% with neurologic sequelae

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8. CYSTICERCOSIS (pp. 1130–1131)

• Caused by larval stage of Taenia solium (pork tapeworm)
• Humans are intermediate hosts (ingest eggs from contaminated food/water/fecal-oral from tapeworm carrier)
• Most common preventable cause of epilepsy in developing world

Neurocysticercosis

• Most common and serious form
• Cysts in brain parenchyma, ventricles, subarachnoid space, spinal cord
• Clinical: new-onset seizures in adult (most common presentation), headache, hydrocephalus, focal deficits
• CT: calcified granulomas (inactive); ring-enhancing lesions with edema (active)
• MRI superior to CT
• Serology: EITB (enzyme-linked immunoelectrotransfer blot) - most specific

Treatment

• Antiparasitic: Albendazole (preferred) + Praziquantel
• Steroids (dexamethasone) - essential with antiparasitic to prevent inflammatory reaction
• Antiepileptics for seizure control
• Surgical CSF diversion for obstructive hydrocephalus
• Inactive calcified cysts: antiparasitic NOT indicated; treat seizures only

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9. AMERICAN TRYPANOSOMIASIS (Chagas Disease) (p. 1131)

• Caused by Trypanosoma cruzi
• Vector: reduviid bug ("kissing bug") - bites near mouth/eyes at night, defecates in wound
• Endemic in Latin America
• Also transmitted via blood transfusion, organ transplant, vertical (mother to child)

Phases

• Romaña's sign: unilateral painless periorbital edema at site of conjunctival inoculation
• Chagoma: indurated skin lesion at inoculation site
• Fever, malaise, lymphadenopathy, hepatosplenomegaly
• Myocarditis (can be fatal in children)

• Cardiomyopathy (most lethal) - arrhythmias, heart block, sudden death
• Megaesophagus (dysphagia) and megacolon (constipation, obstruction)
• Diagnosis: Giemsa stain of blood (acute); serology (chronic)

Treatment

• Benznidazole or Nifurtimox (most effective in acute phase)
• Chronic phase: treat complications (pacemaker, surgery)

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10. LEISHMANIASIS (VISCERAL) (pp. 1132–1133)

• Caused by Leishmania donovani complex
• Vector: female sandfly (Phlebotomus in Old World, Lutzomyia in New World)
• Also called Kala-azar ("black fever" in Hindi)

Clinical Features

• Incubation: weeks to months
• Classic triad: prolonged fever + massive splenomegaly + weight loss
• Hepatomegaly, lymphadenopathy
• Hyperpigmentation of skin (kala-azar = black fever)
• Pancytopenia (leukopenia, anemia, thrombocytopenia)
• Hypergammaglobulinemia

Diagnosis

• Splenic aspirate (most sensitive, risky) or bone marrow biopsy showing Leishman-Donovan bodies (amastigotes)
• rK39 antigen test (rapid diagnostic test; high specificity)
• Serology (ELISA)

Treatment

• Liposomal amphotericin B (drug of choice in immunocompromised/pregnancy)
• Miltefosine (oral; not in pregnancy)
• Meglumine antimoniate / sodium stibogluconate (pentavalent antimonials) - traditional but toxic
• Without treatment: >95% mortality

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11. SCHISTOSOMIASIS (Bilharzia / Snail Fever) (p. 1133)

• Caused by Schistosoma species (S. mansoni, S. haematobium, S. japonicum)
• Intermediate host: freshwater snails
• Cercariae penetrate intact skin during freshwater contact

Phases

• Swimmer's itch: cercarial dermatitis at skin penetration
• Katayama fever (acute): 4–8 weeks after exposure - fever, urticaria, eosinophilia, hepatosplenomegaly
• Chronic: hepatic fibrosis (periportal "pipestem" fibrosis), portal hypertension, esophageal varices (S. mansoni); hematuria and bladder cancer (S. haematobium)

Diagnosis

• Stool or urine microscopy (ova)
• Serology
• Eosinophilia - important clue

Treatment

• Praziquantel (drug of choice for all species)

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12. ZIKA VIRUS (Cross-reference, p. 1126)

• CDC recommendations: Men returning from Zika-risk areas wait 3 months before unprotected sex; women wait 2 months (even if asymptomatic)
• Treatment: supportive

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PART 2: VIVA QUESTIONS

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SECTION A - HIGH-YIELD VIVA QUESTIONS

Zoonoses & Anthrax

• 95% are cutaneous; characteristic lesion is a painless black eschar preceded by pruritic macule → serosanguinous vesicles

• Naturally acquired: penicillin or amoxicillin × 3–7 days
• Bioterrorism: ciprofloxacin × 60 days (doxycycline as alternative)

• Chronic skin granuloma caused by Mycobacterium marinum; associated with fish tank exposure

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Chikungunya

• Both: Aedes vector, fever, rash, thrombocytopenia
• Chikungunya: severe debilitating polyarthralgia/arthritis (often chronic), hemorrhagic complications RARE
• Dengue: hemorrhagic manifestations more prominent, plasma leakage/shock in severe cases

• Chronic polyarthritis/arthralgia lasting months to years (post-chikungunya arthritis)

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Relapsing Fever

• During a febrile period - spirochetes are most abundant in blood during febrile episodes

• Ceftriaxone (first-line for CNS involvement); doxycycline/tetracycline for uncomplicated cases

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Yellow Fever

• Relative bradycardia despite high fever (pulse-temperature dissociation); seen in yellow fever

• Eosinophilic intracytoplasmic inclusions representing apoptotic hepatocytes in yellow fever

• "Black vomit" (hematemesis), jaundice, oliguria/renal failure, and rapid deterioration after brief remission ("period of intoxication")

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Ebola / Marburg

• Fruit bats (Pteropodidae family)

• Negative-pressure room + HEPA respirators + gloves + gowns + contact public health immediately

• 2–21 days - important for quarantine duration; contacts must be monitored for 21 days

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Crimean-Congo Hemorrhagic Fever

• Hyalomma ticks (hard ticks); treatment is ribavirin

• Prehemorrhagic (days 1–3): fever, headache, myalgias
• Hemorrhagic (days 3–6): petechiae, ecchymoses, severe bleeding
• Convalescence (week 2 onward, if survived)

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Lassa Fever

• Reservoir: Mastomys rat (multimammate rat); transmitted via rat urine/droppings (not primarily person-to-person like Ebola)

• Sensorineural hearing loss (affects ~25% of survivors)

• AST >150 IU/L is associated with poor prognosis

• Ribavirin (most effective when given early; IV preferred)

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Japanese Encephalitis

• Vector: Culex mosquito (breeds in rice paddies); reservoir: pigs and wading birds

• Bilateral thalamic lesions (high signal on T2/FLAIR)

• Mask-like facies, cogwheel rigidity, tremor - due to basal ganglia involvement

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Cysticercosis

• Neurocysticercosis (Taenia solium)
• Calcified (inactive) cysts: antiepileptics only; NO antiparasitic
• Active cysts: Albendazole + steroids (dexamethasone) + antiepileptics

• Dying cysts release antigens causing intense inflammatory reaction that can worsen cerebral edema and seizures; steroids prevent this

• EITB (enzyme-linked immunoelectrotransfer blot)

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Chagas Disease

• Unilateral painless periorbital edema (swelling of eyelid) due to conjunctival inoculation of Trypanosoma cruzi by reduviid bug - indicates acute Chagas disease

• Chagasic cardiomyopathy (arrhythmias, heart block, sudden death, dilated cardiomyopathy)
• Megaesophagus (dysphagia, regurgitation)
• Megacolon (constipation, volvulus)

• Benznidazole or Nifurtimox; most effective in acute phase (cure rate >80%); much less effective in chronic phase

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Visceral Leishmaniasis (Kala-azar)

• Prolonged fever + massive splenomegaly + weight loss (+ hyperpigmentation = "black fever")

• Liposomal amphotericin B (miltefosine is contraindicated in pregnancy; antimonials have significant toxicity)

• Splenic aspirate (most sensitive ~98%, but risk of hemorrhage)
• Bone marrow biopsy (safer, sensitivity ~85%): demonstrates Leishman-Donovan bodies (amastigotes inside macrophages)

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Schistosomiasis

• Acute hypersensitivity reaction to migrating schistosome larvae; occurs 4–8 weeks after initial exposure; features: fever, urticaria, eosinophilia, hepatosplenomegaly

• Praziquantel (single drug for all species: S. mansoni, S. haematobium, S. japonicum)

• S. haematobium → chronic bladder inflammation → squamous cell carcinoma of bladder

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SECTION B - SHORT ANSWER VIVA QUESTIONS

• Aedes species (A. aegypti, A. albopictus)

• Visceral leishmaniasis; named for hyperpigmentation of skin due to adrenal involvement and melanin stimulation

• Lassa fever, CCHF, Hantavirus pulmonary syndrome

• Cercarial penetration (swimmer's itch) → Katayama fever 4–8 weeks later when eggs are laid

• Yellow fever - live attenuated vaccine; Japanese encephalitis - inactivated vaccine

• For calcified (dead) cysts - treat only the seizures; giving albendazole for inactive cysts provides no benefit and may cause inflammation

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QUICK REFERENCE SUMMARY TABLE

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Note: The page markers in the digital library confirmed Block 13 (pp. 1049–1125) and Block 14 (pp. 1126–1196) of the Tintinalli 9th edition database. All content above is drawn directly from the retrieved textbook blocks.

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Tintinalli's Emergency Medicine 9th Edition - Chapter 167

STROKE SYNDROMES

PG Notes & Viva Questions

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SECTION 1: INTRODUCTION & EPIDEMIOLOGY

• 795,000 strokes per year in the USA (one every 40 seconds; one death every 4 minutes)
• 77% primary strokes; 23% recurrent strokes
• Financial burden: $33.9 billion (2012-2013)
• Age-adjusted stroke death rate fell 28.7% (2004-2014)
• Treatments driving improvement: stroke units, thrombolysis, mechanical thrombectomy, expanding treatment windows

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SECTION 2: PATHOPHYSIOLOGY & ANATOMY

Definition

Stroke Types & Proportions

Ischemic Stroke - Causes

1. Thrombotic - in situ thrombus on atherosclerotic plaque
2. Embolic - cardioembolism (AF, valvular disease), artery-to-artery embolism
3. Hypoperfusion - systemic hypotension, cardiac arrest

Vascular Anatomy

• Anterior circulation: Internal carotid artery (ICA) → Middle cerebral artery (MCA) + Anterior cerebral artery (ACA)
• Posterior circulation: Vertebral arteries → Basilar artery → Posterior cerebral artery (PCA), PICA, AICA, SCA
• Clinical findings determined by location of lesion + degree of collateral circulation

Ischemic Penumbra

• Core of dead neurons surrounded by ischemic penumbra (viable but at-risk tissue)
• Neurons die within minutes of complete cessation of perfusion
• Treatment goal: rapid reperfusion to salvage penumbra

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SECTION 3: PREHOSPITAL CARE

Prehospital Stroke Scales (Table 167-3)

Large Vessel Occlusion (LVO) Detection

• Multiple prehospital scales developed (none with high specificity AND sensitivity)
• No single prehospital LVO scale recommended for routine use yet
• Goal: route LVO patients to comprehensive stroke centers capable of thrombectomy

Key Prehospital Actions

• Rapid recognition and transport ("time is brain")
• Pre-notification of receiving hospital
• Establish time of last known well (LKW) - most critical piece of information
• IV access, ECG monitoring, glucose check

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SECTION 4: CLINICAL FEATURES - ISCHEMIC STROKE SYNDROMES

General Principles

• Stroke = sudden onset neurologic deficit
• Location of lesion determines clinical syndrome
• NIHSS (National Institutes of Health Stroke Scale) = standard severity quantification

NIHSS Scoring (Table 167-6)

• 0 = no deficit
• 1-4 = minor stroke
• 5-15 = moderate stroke
• 16-20 = moderate-severe
• 21-42 = severe stroke

A. Anterior Circulation Strokes

1. Middle Cerebral Artery (MCA) - Most Common

• Contralateral hemiplegia (face and arm > leg)
• Contralateral hemisensory loss
• Homonymous hemianopia
• Gaze deviation toward the lesion ("eyes look at the stroke")
• Dominant hemisphere (usually left): Aphasia (Broca's = expressive; Wernicke's = receptive; Global = both)
• Non-dominant hemisphere (usually right): Neglect, anosognosia, constructional apraxia
• Superior division MCA: Broca's aphasia + arm weakness
• Inferior division MCA: Wernicke's aphasia + visual field defect
• Large MCA territory stroke → malignant MCA syndrome (massive edema, herniation)

2. Anterior Cerebral Artery (ACA)

• Contralateral leg weakness > arm (reversed from MCA)
• Frontal lobe signs: abulia, urinary incontinence, personality change
• Grasp reflex

3. Internal Carotid Artery (ICA)

• Variable depending on collaterals; can mimic large MCA or combined MCA+ACA territory
• Ipsilateral monocular blindness (amaurosis fugax if TIA) - from ophthalmic artery

B. Posterior Circulation Strokes

1. Posterior Cerebral Artery (PCA)

• Contralateral homonymous hemianopia (most common) - with macular sparing
• Cortical blindness (bilateral PCA)
• Thalamic involvement: hemisensory loss, thalamic pain syndrome
• Dominant: alexia without agraphia, anomia

2. Basilar Artery (most dangerous)

• "Locked-in syndrome": quadriplegia + anarthria + preserved consciousness; only vertical eye movements preserved
• Coma (if tegmentum involved)
• Cranial nerve palsies + contralateral long tract signs = "crossed signs" (hallmark of brainstem stroke)
• Diplopia, dysarthria, dysphagia, vertigo, ataxia

3. PICA (Posterior Inferior Cerebellar Artery) - Lateral Medullary Syndrome (Wallenberg's)

• Ataxia (ipsilateral limb/gait)
• Ipsilateral Horner's syndrome (ptosis, miosis, anhidrosis)
• Ipsilateral facial pain/numbness (descending trigeminal)
• Vertigo, nausea, vomiting, hiccups, dysphagia
• Dissociated sensory loss: ipsilateral face + contralateral body (spinothalamic)
• NO hemiplegia (corticospinal tracts spared)

4. AICA (Anterior Inferior Cerebellar Artery)

• Lateral inferior pontine syndrome
• Ipsilateral: facial weakness, facial numbness, deafness/tinnitus (cochlear involvement), Horner's
• Contralateral: body pain/temperature loss

5. Cerebellar Stroke

• Sudden onset vertigo, nausea, vomiting, truncal ataxia, inability to walk
• Headache common
• CRITICAL: Cerebellar edema → obstructive hydrocephalus → tonsillar herniation (life-threatening)
• May be initially misdiagnosed as labyrinthitis
• Distinguishing from labyrinthitis: inability to walk, direction-changing nystagmus, HINTS exam

6. Lacunar Infarcts

• Small vessel disease in basal ganglia, thalamus, internal capsule, pons
• Classic syndromes:
  • Pure motor hemiplegia (posterior limb of internal capsule/basis pontis)
  • Pure sensory stroke (thalamus - VPL nucleus)
  • Ataxic hemiparesis (posterior limb of internal capsule/pons)
  • Dysarthria-clumsy hand (pons/genu of internal capsule)
  • Sensorimotor stroke (thalamocapsular)

C. Transient Ischemic Attack (TIA)

• Traditional definition: focal neurologic deficit lasting <24 hours
• Modern definition (tissue-based): <1 hour, no infarction on DWI
• Two-day stroke risk after TIA: 3-10% (highest in first 24-48 hours)
• ABCD² score for risk stratification:
  • Age ≥60 (1 pt)
  • Blood pressure ≥140/90 (1 pt)
  • Clinical features: unilateral weakness (2), speech without weakness (1)
  • Duration: ≥60 min (2), 10-59 min (1)
  • Diabetes (1)
  • Score 0-3 = low risk; 4-5 = moderate; 6-7 = high

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SECTION 5: HEMORRHAGIC STROKE SYNDROMES

A. Intracerebral Hemorrhage (ICH)

• 10% of all strokes; highest 30-day mortality (~40%)
• Most common causes: hypertension (#1), amyloid angiopathy (#2 in elderly), anticoagulation, AVM, tumor

Hypertensive ICH - Locations

ICH Score (Predicts mortality)

• GCS (3-4 = 2pts; 5-12 = 1pt; 13-15 = 0pts)
• ICH volume ≥30 cm³ (1 pt)
• Intraventricular extension (1 pt)
• Infratentorial origin (1 pt)
• Age ≥80 (1 pt)
• Score 0 = ~0% mortality; Score 5-6 = ~100% mortality

ICH Management

• Airway: Intubate if GCS ≤8 or declining
• BP control: Target SBP <140 mmHg (AHA 2015: 140-150 range acceptable; aggressive lowering to 140 safe but may not improve outcomes vs. 180 target)
• Reverse anticoagulation immediately:
  • Warfarin → Vitamin K + 4-factor PCC (preferred) or FFP
  • Dabigatran → Idarucizumab (Praxbind)
  • Factor Xa inhibitors → Andexanet alfa or 4-factor PCC
  • Heparin → Protamine sulfate
• No role for recombinant Factor VIIa (increases clotting but not outcomes)
• Surgical evacuation: cerebellar hematoma >3 cm or with hydrocephalus/brainstem compression; supratentorial controversial
• ICP management: Head of bed 30°, osmotherapy (mannitol), consider ICP monitor

B. Subarachnoid Hemorrhage (SAH)

• 3% of all strokes; most common cause: ruptured aneurysm (80%)
• Peak age: 40-60 years; females > males
• Risk factors: smoking, hypertension, family history, polycystic kidney disease, connective tissue disorders

Classic Presentation

• "Thunderclap headache": worst headache of life, sudden onset, reaching maximum intensity within seconds to 1 minute
• Neck stiffness, photophobia
• Loss of consciousness at onset in ~50%
• Sentinel headache (warning leak): 10-40% have headache days to weeks before major bleed

Diagnosis

• Non-contrast CT: 98% sensitive within 6 hours; sensitivity drops to ~93% at 24h
• Lumbar puncture: if CT negative but clinical suspicion high - look for xanthochromia (12h-2 weeks after onset) or RBCs that don't clear between tubes
• CT Angiography or conventional digital subtraction angiography (DSA): identify aneurysm

Grading

• Hunt & Hess Scale (clinical): Grade I-V
• Fischer Grade (radiologic on CT): Grade 1-4 (Grade 3 = highest vasospasm risk)

SAH Management

• Nimodipine 60 mg q4h × 21 days (reduces vasospasm-related ischemia; does NOT prevent vasospasm)
• Aneurysm: surgical clipping or endovascular coiling (ISAT trial: coiling preferred for suitable anatomy)
• Prevent rebleeding: early aneurysm repair
• Vasospasm (days 4-14): transcranial Doppler monitoring, Triple-H therapy (hypertension, hypervolemia, hemodilution) - now controversial
• Hydrocephalus: ventriculostomy/EVD
• Avoid aggressive BP lowering until aneurysm is secured

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SECTION 6: STROKE DIAGNOSIS

Imaging

• Non-contrast CT head: FIRST imaging in all acute stroke patients
  • Rules out hemorrhage (before thrombolytics)
  • May be normal in first 6 hours of ischemic stroke
  • Early signs of ischemia: hyperdense MCA sign, loss of insular ribbon, obscuration of lenticular nucleus, sulcal effacement
• CT Angiography (CTA): detects LVO, aneurysm, dissection
• CT Perfusion (CTP): identifies core infarct vs. penumbra - guides thrombectomy selection (DAWN, DEFUSE 3 trials)
• MRI/DWI: Most sensitive for acute ischemia (detects infarct within minutes); gold standard
• MRA: non-invasive vascular imaging

Stroke Mimics (Must exclude)

• Hypoglycemia (check glucose in ALL patients - #1 mimic)
• Todd's paralysis (post-ictal)
• Complicated migraine (hemiplegic migraine)
• Brain tumor
• Hypertensive encephalopathy
• Subdural hematoma
• Bell's palsy (peripheral VII - forehead sparing in central lesion)
• MS exacerbation
• Conversion disorder

Key Lab Tests

• Serum glucose (immediate - must rule out hypoglycemia)
• CBC, coagulation (PT/INR, PTT, platelets)
• BMP, BUN/creatinine
• Type and screen
• ECG (rule out AF; detect cardiac cause; Wellens-like changes in SAH)
• Troponin
• Urine pregnancy test (women of childbearing age)

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SECTION 7: TREATMENT OF ACUTE ISCHEMIC STROKE

General Measures (All patients)

• ABC: Airway, Breathing, Circulation
• IV access × 2, cardiac monitoring, pulse oximetry
• Oxygen: only if SaO₂ <94% (routine supplemental O₂ NOT indicated)
• Glucose: correct hypoglycemia immediately; avoid hyperglycemia (target 140-180 mg/dL)
• Fever: treat aggressively (associated with worse outcomes); use acetaminophen
• Normal saline (not D5W or hypotonic fluids - worsen cerebral edema)
• NPO until swallow evaluation
• Stroke unit admission (proven to reduce complications, length of stay, disability)
• "Drip and ship" if at non-stroke center: give IV tPA then transfer

Blood Pressure Management

Before tPA (if candidate):

• Target: SBP ≤185 / DBP ≤110 mmHg
• Drugs: Labetalol 10-20 mg IV over 1-2 min (repeat ×1) OR Nicardipine infusion 5 mg/h (titrate up by 2.5 mg/h q5-15 min; max 15 mg/h)

After tPA administration:

• Target: SBP <180 / DBP <105 mmHg for 24 hours
• Avoid sudden BP drops (can extend infarct)

In patients NOT receiving tPA:

• Do not lower BP unless SBP >220 or DBP >120 (or other compelling indication like aortic dissection, ACS, hypertensive encephalopathy)
• Permissive hypertension maintains penumbral perfusion
• If BP lowering needed: reduce by no more than 15-25% in first 24 hours

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IV Thrombolysis - Alteplase (rtPA)

Dose

• 0.9 mg/kg IV (max 90 mg)
• 10% as bolus over 1 minute
• Remaining 90% infused over 60 minutes

Time Windows

• 0-3 hours: Eligible if inclusion criteria met (broadest eligibility)
• 3-4.5 hours: Extended window with additional restrictions (Table 167-8)

AHA/ASA 2018 Inclusion Criteria (0-3 hours)

• Diagnosis of acute ischemic stroke with measurable deficit
• Age ≥18 years (no upper age limit for <3h window)
• Onset <3 hours from last known well
• NIHSS: no lower limit (even mild disabling strokes may benefit); no upper limit

Additional Criteria for 3-4.5 Hour Window

• Age >60 years OR no history of both DM AND prior stroke
• NIHSS score ≤25
• No anticoagulant use
• No imaging evidence of ischemic injury >1/3 of MCA territory

Key Exclusion Criteria

• Intracranial hemorrhage on imaging
• SAH symptoms/signs
• Prior intracranial hemorrhage
• Stroke or severe head trauma within 3 months
• Intracranial/intraspinal surgery within 3 months
• GI/urinary tract hemorrhage within 21 days
• SBP >185 / DBP >110 despite treatment
• Platelet count <100,000/mm³
• INR >1.7 / aPTT >40s / PT >15s
• Blood glucose <50 mg/dL (correct first, then reassess)
• Intracranial neoplasm, AVM, or aneurysm
• Aortic arch dissection

Relative Contraindications (use clinical judgment)

• Minor or rapidly improving symptoms (but do not withhold if disabling deficit)
• Seizure at onset (with residual deficit likely from stroke)
• Recent major surgery or trauma within 14 days
• Recent MI within 3 months
• Pregnancy

Complications of tPA

• Symptomatic intracranial hemorrhage: ~6% (vs 0.6% without tPA)
• Systemic hemorrhage
• Angioedema (especially with ACE inhibitors)
• If symptomatic ICH suspected after tPA: STOP infusion, emergent CT, cryoprecipitate (fibrinogen), neurosurgery consult

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Endovascular Thrombectomy (EVT / Mechanical Thrombectomy)

Landmark Trials (all published 2015)

• MR CLEAN, ESCAPE, SWIFT PRIME, EXTEND-IA, THRACE
• All showed dramatic benefit of thrombectomy + standard care vs. standard care alone
• NNT as low as 2.6 to improve functional outcome

Indications (AHA/ASA 2018)

• Proximal LVO (ICA, M1 MCA, basilar)
• NIHSS ≥6
• ASPECTS ≥6 (Alberta Stroke Program Early CT Score - 10-point CT scoring; lower = more infarct)
• Pre-stroke mRS 0-1 (independent)
• Can be treated within 6 hours of symptom onset (Class I, Level A)

Extended Window (6-24 hours) - DAWN & DEFUSE 3 Trials

• DAWN trial: 6-24 hours; clinical-imaging mismatch (small core, large penumbra)
• DEFUSE 3 trial: 6-16 hours; perfusion imaging mismatch
• Patient selection by CTP or MR perfusion imaging
• Now recommended as standard of care for eligible patients

Device

• Stent retrievers (Solitaire, Trevo): most common
• Aspiration catheters (ADAPT technique)
• Often combined

tPA + Thrombectomy

• Give IV tPA if eligible AND plan thrombectomy (do not delay tPA for thrombectomy planning)
• Bridging therapy (tPA then thrombectomy) is standard

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SECTION 8: SPECIAL CIRCUMSTANCES

Stroke with Concurrent Acute MI

• If ST elevation MI: treat both - PCI for MI; thrombolytics or thrombectomy for stroke as appropriate
• Consider cardiology consultation urgently

Cerebellar/Brainstem Stroke Treatment

• Cerebellar hematoma or large infarct with swelling: urgent neurosurgical consultation
• Hydrocephalus from cerebellar stroke: EVD (external ventricular drain)
• Do NOT give anticoagulation acutely in brainstem stroke (risk of hemorrhagic transformation)
• Posterior fossa decompressive surgery for malignant cerebellar edema

Stroke in Special Populations

• Pregnancy: tPA is relatively contraindicated (fetal risk); thrombectomy preferred where available
• Anticoagulated patients: Reverse anticoagulation before tPA if INR >1.7
• Unknown onset/Wake-up stroke: DWI-FLAIR mismatch on MRI predicts recent onset; eligible for tPA (WAKE-UP trial) and thrombectomy

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SECTION 9: SECONDARY STROKE PREVENTION (Initiated in ED)

• Antiplatelet therapy: Aspirin 160-325 mg within 24-48 hours (once hemorrhage excluded and tPA window passed)
• Dual antiplatelet (aspirin + clopidogrel): CHANCE trial - superior to aspirin alone for minor stroke/high-risk TIA (NIHSS ≤3 or ABCD² ≥4) × 21 days, then aspirin alone
• Anticoagulation for AF: Start 3-7 days after moderate stroke; delay in large or hemorrhagic transformation
• Statin therapy: Start high-intensity statin (atorvastatin 80 mg)
• BP control: Long-term target <130/80 mmHg

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SECTION 10: DISPOSITION

• All acute stroke patients: Admit to stroke unit (Class I evidence)
• TIA patients: Admit if ABCD² ≥4, AF, carotid stenosis, or cannot ensure rapid follow-up
• If no stroke unit available: Transfer after stabilization and IV tPA ("drip and ship")
• Telestroke: Remote stroke physician via video can guide tPA decisions at spoke hospitals

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VIVA QUESTIONS - STROKE SYNDROMES (Chapter 167, Tintinalli 9e)

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EPIDEMIOLOGY & PATHOPHYSIOLOGY

• Ischemic: 87%, ICH: 10%, SAH: 3%

• Viable but at-risk brain tissue surrounding the core infarct; target for reperfusion therapy; salvageable if perfused within the time window

• ~1.9 million neurons die per minute during a major stroke; every 15-minute delay in treatment reduces functional independence

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CLINICAL SYNDROMES

• Eyes look toward the lesion in hemispheric stroke (cortical gaze center destroyed, contralateral gaze center pulls eyes toward lesion)
• Eyes look away from lesion (toward hemiplegia) in brainstem/pontine stroke (PPRF destroyed ipsilaterally)

• PICA occlusion; Features: ipsilateral Horner's + ipsilateral facial loss of pain/temperature + ipsilateral limb ataxia + vertigo/dysphagia/hiccups + contralateral body loss of pain/temperature (dissociated sensory loss); NO hemiplegia

• Ventral pons infarction; patient is quadriplegic and anarthric but conscious; only vertical eye movements preserved (intact midbrain); caused by bilateral corticospinal/corticobulbar tract destruction

• Cerebellar infarction (vs. labyrinthitis); dangerous complication = cerebellar edema → obstructive hydrocephalus → tonsillar herniation → death

1. Pure motor hemiplegia (posterior limb internal capsule/basis pontis)
2. Pure sensory stroke (thalamic VPL)
3. Ataxic hemiparesis (pons/internal capsule)
4. Dysarthria-clumsy hand syndrome (pons)

• Transient neurologic deficit lasting <1 hour with no evidence of infarction on DWI-MRI

• Predicts 2-day stroke risk after TIA; score 6-7 = high risk (~8%); score 0-3 = low risk (~1%)

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DIAGNOSIS

• Hyperdense MCA sign (thrombus in MCA)
• Loss of insular ribbon
• Obscuration of lenticular nucleus
• Sulcal effacement
• Note: CT may be normal in first 6 hours of ischemic stroke

• Alberta Stroke Program Early CT Score (0-10): 10 = normal; lower scores = more infarct burden; score <6 associated with poor outcomes from thrombectomy (relative contraindication)

• Blood glucose - hypoglycemia is the #1 stroke mimic and must be excluded immediately

• Head Impulse, Nystagmus, Test of Skew; used to distinguish central (stroke) from peripheral (vestibular neuritis) cause of acute vestibular syndrome
• Central stroke: normal head impulse + direction-changing nystagmus + skew deviation = 100% sensitive for posterior fossa stroke (more sensitive than early MRI)

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THROMBOLYSIS (HIGH-YIELD)

• 0.9 mg/kg (max 90 mg); 10% as IV bolus over 1 min; remaining 90% over 60 min

• Must lower BP first: target SBP ≤185 / DBP ≤110; use labetalol 10-20 mg IV or nicardipine infusion; once BP controlled, tPA can be given (age is not an exclusion)

• SBP <180 / DBP <105 mmHg for first 24 hours post-tPA

• Any intracranial hemorrhage on imaging
• Prior intracranial hemorrhage history
• Stroke or severe head trauma within 3 months
• Platelet count <100,000/mm³
• Blood glucose <50 mg/dL (before correction)
• INR >1.7
• Aortic arch dissection

• No upper or lower limit in the 0-3 hour window; both mild disabling strokes and very severe strokes may benefit; rapidly improving symptoms are a relative (not absolute) contraindication

• Stop tPA infusion; this is tPA-associated angioedema (especially with concurrent ACE inhibitor use); manage airway urgently; give antihistamines, steroids, epinephrine as needed

• Stop infusion immediately
• Urgent CT head
• Cryoprecipitate (provides fibrinogen; 10 units IV)
• Neurosurgery consult
• Consider TXA (tranexamic acid), FFP

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MECHANICAL THROMBECTOMY

• MR CLEAN, ESCAPE, SWIFT PRIME, EXTEND-IA, THRACE

• LVO (ICA, M1 MCA, basilar)
• NIHSS ≥6
• ASPECTS ≥6
• Pre-stroke mRS 0-1
• Treatable within 6 hours

• DAWN (6-24 hours): clinical-imaging mismatch
• DEFUSE 3 (6-16 hours): perfusion imaging mismatch

• No - give IV tPA if eligible (bridging therapy); do not delay tPA to plan thrombectomy

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HEMORRHAGIC STROKE

• Putamen (most common): contralateral hemiplegia, eyes deviated toward lesion
• Thalamus: hemisensory, "setting sun" eye deviation (downward)
• Cerebellum: ataxia, vomiting, risk of herniation
• Pons: pinpoint pupils, quadriplegia, fever, coma (worst prognosis)

• SBP <140 mmHg (AHA 2015); achievable target of 140-150 range; aggressive lowering to 140 is safe but functional benefit over 180 target remains debated

• 4-factor PCC (Kcentra) - preferred (rapid, complete reversal, less volume than FFP)
• PLUS Vitamin K 10 mg IV (for sustained reversal)
• NOT FFP alone (volume, time issues)

• Idarucizumab (Praxbind) - specific reversal agent for dabigatran

• Scores GCS, ICH volume ≥30 cm³, intraventricular extension, infratentorial origin, age ≥80; predicts 30-day mortality; Score 5-6 = ~100% mortality

• Cerebellar hematoma >3 cm or with brainstem compression/hydrocephalus = urgent surgery
• Supratentorial: controversial; STICH trials showed no clear benefit for routine surgery

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SAH

• "Thunderclap headache" - worst headache of life, instantaneous onset reaching maximum intensity within seconds; ± loss of consciousness, neck stiffness, photophobia

• Lumbar puncture: look for xanthochromia (yellow discoloration of CSF from RBC breakdown) - reliable from 12 hours to 2 weeks after onset; also RBCs that don't clear between tubes 1 and 4

• Nimodipine 60 mg every 4 hours × 21 days (oral/NG); reduces ischemic complications from vasospasm (does NOT prevent vasospasm itself)

• ISAT trial: endovascular coiling superior to surgical clipping for suitable anatomy (improved independence at 1 year)

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SPECIAL SCENARIOS

• "Wake-up stroke" - use DWI-FLAIR mismatch on MRI (DWI bright + FLAIR normal = infarct <4.5 hours old); eligible for tPA (WAKE-UP trial) or thrombectomy if LVO present (DAWN/DEFUSE 3 criteria)

• IV tPA given at a primary stroke center (spoke) while arranging transfer to a comprehensive stroke center (hub) for thrombectomy evaluation; "drip and ship" vs. "mothership" (direct transfer without tPA) debate ongoing

• Dual antiplatelet: Aspirin + clopidogrel (CHANCE trial) for 21 days, then aspirin alone; reduces 90-day stroke risk by ~32%

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QUICK REFERENCE TABLES

Stroke Type vs. Key Features

tPA Time Windows

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Tintinalli's Emergency Medicine 9th Edition — Chapter 138

SEIZURES IN INFANTS AND CHILDREN

PG Notes & Viva Questions

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PART 1: COMPREHENSIVE NOTES

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1. INTRODUCTION & EPIDEMIOLOGY

• Seizures account for many paroxysmal events in children, but ≥30% of paroxysmal events presenting to the ED are misdiagnosed as seizures
• Prevalence: ~1% of children up to age 14 years
• Highest incidence in children <1 year old (120 cases per 100,000)
• Febrile seizures: most common type; affect 3–4% of children aged 6 months to 5 years
• Epilepsy = recurrent unprovoked seizures; affects ~326,000 American children <15 years; lifetime prevalence ~1%
• Status epilepticus incidence: 18–23 per 100,000 in developed countries; higher in younger children
• Most seizure activity stops before the child reaches the ED → history is paramount

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2. PATHOPHYSIOLOGY

• Seizures = abnormal, excessive, paroxysmal neuronal activity in the brain (primarily cortex)
• Glutamate (excitatory): activates NMDA receptors → initiates and propagates seizure activity
• GABA (inhibitory): failure of GABA inhibition → facilitates seizure spread
• Why children are more susceptible:
  • Incomplete myelination limits secondary generalization in young infants
  • Relative imbalance between glutamate and GABA
  • Paradoxical excitation from GABA in younger children (GABA is excitatory early in development due to high intracellular Cl⁻)

Seizure Classification

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3. TYPES OF SEIZURES (Clinical Features)

A. Generalized Seizures

B. Focal (Partial) Seizures

C. Important Pediatric Epilepsy Syndromes

1. Infantile Spasms (West Syndrome)

• Age: 4–8 months (peak)
• Classic triad: infantile spasms + hypsarrhythmia (EEG) + developmental regression
• Spasms: brief symmetric flexion/extension ("salaam attacks"); occur in clusters on awakening
• EEG: hypsarrhythmia (chaotic high-amplitude slow waves with multifocal spikes)
• Causes: tuberous sclerosis, Down syndrome, structural brain lesions
• Treatment: ACTH or vigabatrin (infantile spasms associated with tuberous sclerosis)

2. Lennox-Gastaut Syndrome

• Age: 1–8 years
• Triad: multiple seizure types + slow spike-wave EEG (1.5–2.5 Hz) + intellectual disability
• Seizure types: tonic, atonic, absence; tonic-clonic
• Treatment resistant; poor prognosis
• Drugs: valproate, lamotrigine, rufinamide, clobazam

3. Childhood Absence Epilepsy (CAE)

• Age: 4–12 years; girls > boys
• Multiple brief absence seizures per day (can be 50–100/day)
• EEG: 3 Hz generalized spike-wave
• Treatment: ethosuximide (drug of choice), valproate, lamotrigine
• Good prognosis; usually remits by puberty

4. Juvenile Myoclonic Epilepsy (JME)

• Age: 12–18 years
• Morning myoclonic jerks (particularly after sleep deprivation/alcohol)
• Associated tonic-clonic seizures
• EEG: 4–6 Hz polyspike-wave
• Treatment: valproate (first line); levetiracetam; lifelong treatment usually needed

5. Benign Rolandic Epilepsy (BECTS)

• Age: 3–13 years
• Focal seizures involving face/mouth (unilateral facial twitching, drooling, dysarthria); often nocturnal
• EEG: centrotemporal spikes
• Self-limited; resolves by adolescence; often no treatment needed

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4. HISTORY (Key Points - Table 138-1)

• Onset: Was the child awake, asleep, or waking?
• Description: Duration, motor activity (focal vs. generalized), automatisms, eye deviation, color change
• Postictal state: duration, focal weakness (Todd's paralysis)
• Prior seizures: first episode or recurrence?
• Fever: temperature, duration, source
• Possible triggers: sleep deprivation, illness, missed medications
• Prenatal/perinatal history: birth complications, neonatal seizures
• Developmental history: milestones, regression
• Family history: febrile seizures, epilepsy
• Medications: current AEDs, recent changes; possible ingestion/toxin
• Trauma: even if denied (consider non-accidental trauma)

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5. PHYSICAL EXAMINATION

• Vital signs: temperature (fever source), HR, RR, BP, SpO₂
• Head: fontanelle (bulging = ↑ICP), head circumference, bruises/trauma
• Eyes: papilledema, retinal hemorrhages (non-accidental trauma), pupil response
• Skin: café-au-lait spots (NF1), ash-leaf macules (tuberous sclerosis), port-wine stain (Sturge-Weber), petechiae/purpura (meningococcemia)
• Neurologic: mental status (return to baseline?), focal deficits, Todd's paralysis (transient focal weakness post-seizure)
• Signs of infection: meningismus, rash, otitis media

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6. DIFFERENTIAL DIAGNOSIS — Conditions Masquerading as Seizures (Table 138-3)

Key Differentiating Features

• Breath-holding spells: precipitated by pain/frustration → cry → apnea → cyanosis/pallor → brief LOC; self-limited; no postictal phase
• Syncope: prodrome (lightheadedness, nausea), situational triggers, brief tonic/clonic movements can occur but brief; rapid recovery
• Jitteriness (neonates): stimulation-sensitive, stopped by gentle restraint, NO eye deviation; differs from neonatal seizures

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7. LABORATORY TESTING

When to Order (NOT routine for all seizures)

Key Points

• No routine labs for simple febrile seizures (AAP recommendation)
• Lumbar puncture: strongly consider if meningitis signs; consider in infants 6–12 months unimmunized or on antibiotics (may mask meningitis signs)
• Electrolytes: order only if history suggests (vomiting, diarrhea, excessive water intake)

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8. IMAGING

Indications for Emergent CT Head

• Status epilepticus not responding to treatment
• Focal neurologic deficits
• Suspected raised ICP (papilledema, bulging fontanelle)
• Head trauma (especially non-accidental)
• Infants <6 months (higher risk of serious underlying pathology)
• Persistent altered mental status not explained by postictal state

When NOT Required

• Simple febrile seizures (AAP: no imaging needed)
• First-time afebrile seizure with normal exam and return to baseline (MRI outpatient preferable to CT)
• MRI preferred over CT for epilepsy workup (better at detecting cortical dysplasia, mesial temporal sclerosis)

EEG

• Emergent EEG: refractory status epilepticus (especially after RSI/paralysis), suspected nonconvulsive status epilepticus
• Outpatient EEG: most other cases; identifies epilepsy syndromes, guides treatment
• ECG: consider to rule out arrhythmia (long QT) when syncope/arrhythmia is in differential

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9. STATUS EPILEPTICUS (SE)

Definition

• Traditional: continuous seizure activity lasting >30 minutes OR two or more seizures without full recovery of consciousness between them
• Operational/practical (Tintinalli): seizure lasting >5 minutes → treat as SE (because most seizures that will self-terminate do so within 1–3 minutes)

Why SE is an Emergency

• Neuronal injury begins after 30 minutes
• Physiologic consequences: hypoxia, hypercapnia, lactic acidosis, hyperthermia, hypoglycemia, cerebral edema
• Treatment efficacy decreases with time → treat early and aggressively

Causes of SE in Children

• Febrile status epilepticus (most common in young children)
• CNS infection (meningitis, encephalitis)
• Prior epilepsy with breakthrough seizure / subtherapeutic AED
• Metabolic: hypoglycemia, hyponatremia, hypocalcemia
• Toxin/ingestion
• Structural: stroke, trauma, tumor
• Anoxic brain injury

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10. TREATMENT OF SEIZURES / STATUS EPILEPTICUS

General Measures (Immediate)

1. Position: lateral decubitus (recovery position) → prevent aspiration
2. Airway: suction if needed; jaw-thrust/chin-lift; avoid tongue blades (injury risk)
3. Oxygen: 100% O₂ via facemask
4. Monitor: continuous pulse oximetry, cardiac monitoring, capnography if intubated
5. IV/IO access: establish rapidly; if delayed → use alternative routes
6. Bedside glucose: check immediately for ALL afebrile seizures
7. Glucose correction: if hypoglycemic → Dextrose 2–4 mL/kg of D25W (neonates: D10W)
8. Pyridoxine (B6): 100 mg IV in neonates if no other cause identified (pyridoxine-dependent seizures)

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STEP-BY-STEP STATUS EPILEPTICUS PROTOCOL

Phase 1 — FIRST-LINE: Benzodiazepines (0–5 min)

Key rule: Do not delay benzodiazepine for IV access — use IM/IN/rectal route immediately

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Phase 2 — SECOND-LINE: Anti-seizure Medications (5–20 min, if benzodiazepines fail)

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Phase 3 — THIRD-LINE: Refractory Status Epilepticus (>30–60 min)

• Intubation with RSI + continuous EEG monitoring (paralytic masks clinical seizures)
• Continuous infusions (ICU setting):
  • Midazolam infusion: 0.05–2 mg/kg/hr
  • Pentobarbital coma: 5 mg/kg loading dose, then 1–3 mg/kg/hr (goal: burst suppression on EEG)
  • Propofol: caution in children (propofol infusion syndrome risk)
  • Ketamine: 1.5–4.5 mg/kg bolus then infusion (NMDA antagonist; less hemodynamic depression)

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Special Treatments for Specific Causes

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11. FEBRILE SEIZURES

Definition

Incidence: 2–5% of children

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Simple Febrile Seizure (95% of febrile seizures)

Management of Simple Febrile Seizure (AAP Guidelines)

• NO routine blood tests needed
• NO neuroimaging needed
• NO EEG needed
• Evaluate for fever source: urinalysis/culture (especially in infants); throat swab etc.
• Lumbar puncture: strongly consider if ANY signs/symptoms of meningitis; consider in:
  • Infants 6–12 months unimmunized for Hib or S. pneumoniae
  • Children on antibiotics (can mask meningitis signs)
• No anticonvulsant therapy indicated for prevention
• Antipyretics do NOT prevent febrile seizure recurrence (fever is the trigger, not the temperature per se)
• Discharge with parental education

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Complex Febrile Seizure (5% of febrile seizures)

1. Focal seizure
2. Duration >15 minutes (febrile status epilepticus)
3. More than one seizure in 24 hours
4. Abnormal neurologic exam or Todd's paralysis

Management of Complex Febrile Seizure

• More extensive evaluation warranted
• Consider LP (especially if meningismus, ill appearance, very young)
• Consider neuroimaging (MRI preferred)
• EEG (outpatient usually sufficient)
• Pediatric neurology consultation

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Recurrence Risk of Febrile Seizures

• Overall: ~30–50% recurrence
• <12 months old at first seizure: ~50% recurrence risk
• >12 months old at first seizure: ~30% recurrence risk
• Risk factors for recurrence: young age at first seizure, family history, low fever at onset, brief interval from fever onset to seizure

Risk of Developing Epilepsy After Febrile Seizure

• Simple febrile seizure: same as general population (~1% by age 7)
• Complex/multiple febrile seizures + family history + first seizure <12 months: risk up to 7%
• Additional risk factors: developmental delay, focal seizures, Todd's paralysis, abnormal EEG/imaging

Febrile Status Epilepticus

• Febrile seizure lasting >30 minutes
• Most common cause of status epilepticus in young children
• Management: same SE protocol as above
• FEBSTAT study: MRI may show acute hippocampal injury → possible mesial temporal sclerosis later
• Meningitis MUST be excluded (LP after stabilization if no contraindications)

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12. FIRST AFEBRILE SEIZURE

Evaluation

• History and physical examination (most important)
• Bedside glucose (mandatory)
• EEG (outpatient; helps characterize epilepsy syndrome)
• MRI (outpatient preferred over CT; better structural detail)
• Labs only if clinically indicated

Management

• If returns to baseline and exam normal: Discharge with outpatient follow-up (neurology)
• Do NOT routinely start AED after first unprovoked seizure (recurrence risk ~50% at 2 years; starting AED after 2 seizures)
• Exception: start AED if high recurrence risk (structural lesion, abnormal EEG, prior neurologic insult) after neurology consultation

Recurrence Risk after First Unprovoked Seizure

• Overall: 50% recurrence within 2 years
• Higher risk: abnormal EEG, structural brain lesion, focal seizure, prior neurologic insult, status epilepticus as first event

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13. NEONATAL SEIZURES

Definition

Importance

• Highest seizure incidence of any age group
• Reflect serious underlying pathology
• Clinical manifestations are subtle and atypical (different from older children)

Clinical Manifestations

Jitteriness (most common neonatal movement to confuse with seizures):

• Stimulus-sensitive
• Stopped by gentle restraint
• No eye deviation
• No autonomic changes
• Abnormal EEG NOT seen

Causes of Neonatal Seizures (in order of frequency)

1. Hypoxic-ischemic encephalopathy (HIE) — #1 cause (50–65%)
2. Intracranial hemorrhage (IVH, subdural, SAH)
3. Ischemic stroke
4. Metabolic: hypoglycemia (#1 treatable cause), hypocalcemia, hypomagnesemia, hyponatremia, pyridoxine deficiency
5. CNS infection: meningitis, encephalitis (HSV especially)
6. Inborn errors of metabolism: organic acidemias, urea cycle defects
7. Drug withdrawal: neonatal abstinence syndrome (opioids, benzodiazepines)
8. Structural/genetic: brain malformations, trisomies

Workup for Neonatal Seizures

• Bedside glucose (immediate)
• Electrolytes: Na, Ca, Mg, phosphorus
• CBC, blood culture
• Blood gas, lactate, ammonia
• LFTs, coagulation studies
• LP (after stabilization): cell count, glucose, protein, Gram stain, culture, HSV PCR
• Urine: organic acids, amino acids; drug screen
• Head ultrasound (rapid, portable, no radiation - good for IVH)
• CT head: acute hemorrhage
• MRI brain (if stable): best for HIE, stroke, cortical malformations
• EEG: essential - many neonatal seizures are electrographic only (no clinical correlate, especially after treatment)
• Pyridoxine challenge: 100 mg IV if refractory neonatal seizures

Treatment of Neonatal Seizures

• Treat underlying cause first (glucose, calcium, magnesium)
• Phenobarbital: first-line AED (20 mg/kg IV loading dose)
• Phenytoin/fosphenytoin: second line (20 mg/kg IV)
• Levetiracetam: increasing use (well tolerated; 40–60 mg/kg IV)
• Pyridoxine: 100 mg IV if no cause found / refractory
• Midazolam infusion for refractory neonatal SE
• Benzodiazepines: less effective in neonates (GABA paradox); phenobarbital preferred

Note: After paralytic/RSI in any child — must use EEG to monitor for ongoing seizures

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14. SEIZURES IN SPECIAL POPULATIONS

A. Children with Known Epilepsy (Breakthrough Seizures)

• Check AED levels (subtherapeutic?)
• Identify precipitants: illness, fever, sleep deprivation, missed doses, drug interactions
• Do NOT change AED regimen without neurology input
• Discharge if: back to baseline, drug levels corrected, follow-up arranged

B. Seizures in Children with VP Shunts

• Shunt malfunction → ↑ ICP → seizure
• Evaluate for shunt malfunction: CT head (ventricular size), shunt series X-ray, neurosurgery consultation
• Do NOT assume seizure is simply from epilepsy without ruling out shunt failure

C. Post-traumatic Seizures

• Immediate (<24 hours): direct effect of trauma; usually self-limited
• Early (1–7 days): treat with AED (phenytoin/levetiracetam)
• Late (>7 days): risk factor for epilepsy development
• Concern for non-accidental trauma (NAT): retinal hemorrhages, subdural hematoma, rib fractures → mandatory reporting

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15. DISPOSITION

Discharge Criteria

• Infants >6 months with simple febrile seizure (fever source identified/managed)
• First-time seizure <15 min, returned to baseline, normal exam, no secondary cause
• Follow-up with PCP or pediatric neurology arranged

Admission Criteria

• Status epilepticus
• Seizure with CNS infection (meningitis, encephalitis)
• Toxic/metabolic cause not corrected
• Neonatal seizures (all)
• Not returned to baseline
• Significant underlying pathology identified
• Refractory seizures requiring continuous infusions → ICU

Parental Education (Discharge)

• No bathing/swimming alone (drowning risk)
• Shower without locking door
• No driving until neurologist clears
• Seizure first aid: lateral position, do not restrain, do not put anything in mouth
• When to call EMS: seizure >5 min, second seizure, not waking up

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PART 2: VIVA QUESTIONS

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SECTION A - EPIDEMIOLOGY & PATHOPHYSIOLOGY

• Febrile seizures (3–4% of all children aged 6 months to 5 years)

• Incomplete myelination; relative imbalance between excitatory (glutamate) and inhibitory (GABA) neurotransmitters; GABA is paradoxically excitatory in neonates/young infants due to high intracellular chloride concentration

• 18–23 per 100,000; higher in younger children

• Recurrent unprovoked seizures (2 or more unprovoked seizures >24 hours apart, OR one unprovoked seizure with ≥60% recurrence risk)

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SECTION B - TYPES OF SEIZURES & SYNDROMES

• Classic triad: infantile spasms + hypsarrhythmia on EEG + developmental regression; age 4–8 months; spasms occur in clusters ("salaam attacks"); treatment: ACTH or vigabatrin (vigabatrin preferred for tuberous sclerosis)

• West: hypsarrhythmia (chaotic high-amplitude multifocal spike-wave)
• Lennox-Gastaut: slow spike-wave at 1.5–2.5 Hz

• Ethosuximide - most effective; safest profile; valproate also effective but more side effects; lamotrigine third option

• Lennox-Gastaut syndrome (atonic seizures = drop attacks); also Doose syndrome (myoclonic-atonic epilepsy)

• Benign Rolandic epilepsy (BECTS): children 3–13 years; facial/oropharyngeal focal seizures; centrotemporal spikes on EEG; nocturnal predominance; self-limited (resolves by adolescence), often no treatment needed

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SECTION C - DIAGNOSIS & DIFFERENTIAL

• ≥30% are non-seizure events

• Breath-holding spells: provoked by pain/fear/frustration → cry → apnea → cyanosis or pallor → brief LOC/stiffening; no postictal phase; EEG normal; self-limiting; no treatment needed
• Seizures: no consistent provocant, postictal drowsiness, EEG may be abnormal

• Jitteriness: stimulation-sensitive, stopped by gentle restraint, NO eye deviation, NO autonomic changes, normal EEG
• Neonatal seizures: NOT stopped by restraint, eye deviation common, EEG abnormal, autonomic changes (HR, BP changes)

• Transient focal neurologic weakness (typically motor) following a focal seizure; lasts minutes to hours; NOT a new stroke; resolves spontaneously; indicates seizure originated contralateral to the weak limb

• Any signs/symptoms of meningitis (mandatory)
• Infants 6–12 months who are unimmunized for Hib or S. pneumoniae
• Children currently on antibiotics (may mask meningitis signs)
• Complex febrile seizure with ill appearance

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SECTION D - TREATMENT (HIGH-YIELD)

• IV/IO: Lorazepam 0.1 mg/kg
• IM: Midazolam 0.2 mg/kg (RAMPART trial showed equal efficacy to IV lorazepam)
• Intranasal: Midazolam 0.2 mg/kg (via mucosal atomization device)
• Buccal: Midazolam 0.3 mg/kg
• Rectal: Diazepam 0.5 mg/kg (home/EMS rescue)

• IM midazolam (0.2 mg/kg) was non-inferior to IV lorazepam for pediatric status epilepticus; IM midazolam achieved faster time to treatment (no IV access needed) and had similar seizure cessation rates

• Prolonged seizures cause internalization of GABA-A receptors → loss of surface GABA receptors → reduced response to benzodiazepines and other GABAergic drugs; also receptor trafficking changes; excitotoxic damage becomes self-perpetuating

• 20 mg phenytoin equivalents (PE)/kg IV or IM, infused over 7–10 min; advantage over phenytoin: can give IM, less cardiac toxicity, can infuse faster, less injection-site reactions

• Check phenytoin level (subtherapeutic?)
• Identify precipitant (fever, illness, missed doses)
• Treat active seizure with benzodiazepine if ongoing
• Do NOT alter medication regimen without neurology
• Discharge if returned to baseline + levels corrected

• Children: D25W 2–4 mL/kg IV (= 0.5–1 g/kg dextrose)
• Neonates: D10W 2 mL/kg IV (D25W too hypertonic for neonates)
• Check glucose before giving phenytoin (phenytoin precipitates in dextrose solutions)

• Give 100 mg IV to all neonates with unexplained refractory seizures; some rare genetic disorders (pyridoxine-dependent epilepsy - ALDH7A1 mutation) are only responsive to pyridoxine; safe empiric treatment

• 3% hypertonic saline: 3–5 mL/kg IV over 10–15 min; goal is to raise sodium by 3–5 mEq/L to stop seizures (not to fully correct sodium)

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SECTION E - FEBRILE SEIZURES

• Generalized tonic-clonic seizure, <15 min, single episode in 24 hours, fever ≥38°C, age 6 months–6 years, normal post-ictal neuro exam
• Workup: NONE routinely (AAP); focus only on fever source

• Any of: focal seizure, duration >15 min, recurrence within 24 hours, abnormal neurologic exam/Todd's paralysis

• No - multiple trials (including the Cochrane systematic review) show antipyretics do NOT prevent febrile seizure recurrence; fever is the trigger but treating fever does not change recurrence risk

• ~1% - same as the general population; no increased risk compared to children without febrile seizures

• This is a complex febrile seizure (focal + >15 min)
• Active seizure: benzodiazepine treatment (lorazepam IV 0.1 mg/kg)
• LP should be strongly considered (young age, unimmunized possibly, complex features)
• Neuroimaging (MRI preferred, not emergent if stabilized)
• EEG (outpatient)
• Pediatric neurology consultation
• Admit for observation

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SECTION F - NEONATAL SEIZURES

• Hypoxic-ischemic encephalopathy (HIE) — accounts for 50–65%

• Phenobarbital (20 mg/kg IV loading dose); if seizure continues after 2 doses, add phenytoin/fosphenytoin or levetiracetam

• In neonates, GABA-A receptor activation causes depolarization (excitation) rather than hyperpolarization (inhibition) due to high intracellular Cl⁻ → GABA is excitatory in neonates; as the brain matures, KCC2 transporter expression increases, Cl⁻ is pumped out, and GABA becomes inhibitory

• Pyridoxine 100 mg IV (empiric trial for pyridoxine-dependent epilepsy); if responds → diagnosis confirmed
• Consider lorazepam, levetiracetam infusion, midazolam infusion
• Send metabolic workup (pyridoxal-5-phosphate, amino acids, organic acids)

• Myoclonic seizures (especially multifocal myoclonic) - associated with severe metabolic disorders, hypoxic-ischemic encephalopathy; high morbidity and mortality

• Focal clonic seizures: NOT stimulus-sensitive, NOT stopped by gentle restraint, EEG shows ictal pattern, eye deviation present
• Jitteriness: stimulus-sensitive, STOPS with restraint, no EEG changes

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SECTION G - SPECIAL POPULATIONS & SCENARIOS

• Shunt malfunction causing obstructive hydrocephalus and raised ICP; evaluate with CT head (ventricular size) + shunt series X-ray; neurosurgery consultation urgently; do not assume it is just a breakthrough seizure from epilepsy

• Immediate (<24 hours): direct effect of trauma; usually benign, self-limited
• Early (1–7 days): treat with AED to prevent seizure-related secondary brain injury
• Late (>7 days): indicates risk of developing post-traumatic epilepsy; long-term AED consideration
• Presence in a child with no clear trauma history → consider non-accidental trauma (NAT)

• After RSI with neuromuscular blockade (paralytic masks convulsive activity)
• Suspected nonconvulsive status epilepticus (altered mental status without clinical seizure activity)
• Refractory status epilepticus (to titrate continuous infusion therapy)

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QUICK SUMMARY TABLE

Pediatric Seizure Management Algorithm

Febrile Seizure At-a-Glance

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Differentiating Thrombotic vs. Embolic vs. Hypoperfusion Stroke

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THE CORE FRAMEWORK

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1. SIDE-BY-SIDE COMPARISON TABLE

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2. MECHANISM IN DETAIL

A. Thrombotic Stroke

• Atherosclerotic plaque builds up in a vessel wall over years
• Plaque rupture or erosion → activates coagulation cascade → in-situ thrombus forms at the site of the damaged vessel
• Lumen progressively narrows → flow decreases → ischemia develops gradually
• Collateral circulation may partially compensate → explains waxing/waning course

• Atherosclerosis (most common)
• Vasculitis
• Arterial dissection
• Polycythemia / hypercoagulable state
• Infection (HIV, syphilis, TB, trichinosis, aspergillosis)

"Transient neurologic deficits in the same vascular distribution suggest underlying vascular disease consistent with a thrombotic stroke" - Tintinalli Ch. 167

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B. Embolic Stroke

• A clot, vegetation, tumor fragment, fat globule, or foreign material forms at a remote site
• It travels through the bloodstream → lodges at a bifurcation or narrows point in the brain
• The vessel wall itself is normal - it is simply plugged from outside
• Embolus may later lyse or fragment → partial reperfusion → hemorrhagic transformation (explains why embolic strokes bleed into infarcts more commonly)
• Fragments may shower into multiple territories simultaneously

"Sudden onset of symptoms suggests an embolic or hemorrhagic stroke" - Tintinalli Ch. 167 "Transient deficits involving different vascular distributions suggest embolism" - Tintinalli Ch. 167

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C. Hypoperfusion Stroke (Watershed / Hemodynamic Infarction)

• No vessel is occluded
• Systemic blood pressure drops (cardiac failure, cardiac arrest, hypovolemia, hypotension during surgery) → global reduction in cerebral perfusion pressure
• The most vulnerable zones are watershed areas - the border zones between territories of two major cerebral arteries - farthest from the heart, last to receive blood
• Two main watershed zones:
  1. Anterior watershed: between ACA and MCA territories → "man in a barrel" syndrome (proximal arm and leg weakness, face spared, language intact)
  2. Posterior watershed: between MCA and PCA territories → visual defects, Balint's syndrome, cortical blindness

• Bilateral, symmetric infarcts along the watershed zones
• "String of pearls" or linear pattern of infarcts on MRI DWI
• No focal arterial occlusion on CTA

"Hypoperfusion stroke: diffuse injury pattern in watershed regions. Symptoms may wax and wane with hemodynamic factors" - Tintinalli Table 167-2

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3. DIFFERENTIATING BY HISTORY (Tintinalli Ch. 167)

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4. DIFFERENTIATING BY IMAGING

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5. DIFFERENTIATING BY CARDIAC WORKUP

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6. CLINICAL SCENARIO EXAMPLES

Scenario 1: Thrombotic Stroke

A 68-year-old hypertensive diabetic man wakes with right arm weakness. He has had 2 prior brief episodes over the last month that resolved fully. Carotid Doppler shows 80% left ICA stenosis. CT is normal; DWI shows left MCA territory infarct.

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Scenario 2: Embolic Stroke

A 72-year-old woman with known AF presents with sudden onset of dense right hemiplegia and global aphasia - reached maximum deficit in seconds. CT shows cortical hypodensity in left MCA territory with hemorrhagic transformation. Echo shows left atrial appendage thrombus.

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Scenario 3: Hypoperfusion Stroke

A 65-year-old man presents 2 days after coronary artery bypass surgery with bilateral arm and shoulder weakness but preserved hand and face function. MRI shows bilateral symmetric DWI restriction along the ACA-MCA watershed. CTA shows no focal occlusion. Intraoperative records show 45 minutes of hypotension.

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7. SUMMARY MNEMONIC

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