01Approach to the Critical Patient/attcp45

Immediate priorities

›Airway and respiratory threat

›Respiratory failure primary cause of death in PSP

›Most fatalities occur within 12 hours of ingestion

›Death rate approximately 6% worldwide; higher in children and developing regions

›Intubation triggers

›Declining NIF below -25 cmH2O

›FVC below 15 mL/kg

›SpO2 falling despite supplemental oxygen

›Inability to count to 20 in one breath

›Dysphagia or inability to manage secretions

›If airway compromise present, immediate RSI preparation

›Succinylcholine with caution given existing flaccid paralysis

›Rocuronium 1.2 mg/kg IV alternative

›Supplemental oxygen for all symptomatic patients

›Target SpO2 >= 94%

›HFNC for hypoxemia without airway threat

Monitoring and escalation

›Monitoring bundle

›Continuous pulse oximetry mandatory

›SpO2 trend is primary escalation trigger

›Serial respiratory rate assessment

›Continuous cardiac telemetry

›Saxitoxin suppresses AV node conduction

›Bradycardia and heart block risk

›Serial respiratory function assessments

›NIF and FVC every 2 to 4 hours in moderate to severe cases

›Rate of progression in first hours is best severity predictor

02History/hx73

Exposure and onset

›Shellfish ingestion history

›Type of shellfish consumed

›Clams and mussels highest risk vectors

›Oysters, scallops, and puffer fish also implicated

›Xanthid crabs and lobster less common vectors

›Source of shellfish

›Recreational or subsistence harvesting highest risk

›Unmonitored coastal areas during algal bloom

›Market-purchased shellfish lower but not zero risk

›Geographic context

›Alaska, Pacific Northwest, Atlantic coast of North America

›Chile, Philippines, parts of Europe

›Red tide or harmful algal bloom advisory in effect

›Timing of symptom onset

›Typical onset 30 to 60 minutes post-ingestion

›Range 30 minutes to 3 hours

›Rapid onset within 30 minutes indicates high toxin load

›Onset greater than 3 hours makes PSP less likely

›Consider alternative diagnoses

›Botulism onset 12 to 36 hours

Symptom progression

›Classic progression pattern

›Perioral paresthesias first

›Tingling and numbness around lips

›Earliest and most consistent finding

›Facial and extremity numbness following

›Tongue and gum numbness

03Physical Exam/exam74

Vital signs and respiratory assessment

›Vital signs snapshot

›Respiratory rate

›Rising rate as respiratory muscle fatigue marker

›Greater than 30 per minute is ominous

›SpO2

›Room air value required

›Declining trend triggers intubation assessment

›Heart rate and blood pressure

›Bradycardia from AV conduction suppression

›Hypotension rare but possible in severe cases

›Temperature

›Typically normal in PSP

›Fever suggests alternative or concurrent diagnosis

›Respiratory function assessment

›Ability to count to 20 in one breath

›Rapid bedside FVC surrogate

›Inability is intubation trigger

›Accessory muscle use

›Sternocleidomastoid recruitment

›Intercostal retractions

›Tidal volume adequacy

›Shallow breathing with normal rate can mask failure

›Negative inspiratory force measurement

›Serial NIF every 2 to 4 hours in moderate to severe cases

›Below -25 cmH2O signals impending failure

Neurological exam

›Sensory findings

04Differential Diagnosis/ddx51

Neurotoxin causes

›Shellfish and marine toxin syndromes

›Tetrodotoxin poisoning

›ICD-10 T61.771

›Nearly indistinguishable from PSP clinically

›Puffer fish ingestion history distinguishes

›Neurotoxic shellfish poisoning

›Brevetoxin from Gulf Coast red tide

›Milder neurologic symptoms

›More prominent gastrointestinal features

›Amnesic shellfish poisoning

›Domoic acid from razor clams and anchovies

›Prominent memory loss and confusion

›Seizures possible

›Ciguatera fish poisoning

›ICD-10 T61.01

›Hot-cold temperature reversal pathognomonic

›Reef fish ingestion not shellfish

›Other neurotoxic exposures

›Organophosphate poisoning

›SLUDGE symptoms (salivation, lacrimation, urination, defecation, GI, emesis)

›Miosis and bradycardia

›Botulism

›ICD-10 A05.1

›Descending paralysis with cranial nerve involvement

›Onset 12 to 36 hours after exposure

›Pupillary dilation distinguishes from PSP

05Laboratory Tests/lt41

Baseline labs for mimic exclusion

›Metabolic and electrolyte panel

›Electrolytes and renal function

›Hyperkalemia or hypokalemia as weakness cause

›Hyponatremia as seizure and weakness cause

›Calcium and magnesium

›Hypocalcemia and hypermagnesemia as neuromuscular causes

›Phosphorus assessment

›Glucose

›Hypoglycemia can mimic neurologic presentations

›Hematology

›Complete blood count

›Baseline hemoglobin for respiratory reserve context

›Leukocytosis if concurrent infection

›Coagulation studies if clinical concern

›Bleeding risk if procedures needed

Respiratory and perfusion monitoring

›Arterial blood gas

›PaCO2 mmHg for ventilatory adequacy

›Rising PaCO2 is intubation trigger

›Respiratory acidosis indicates failure

›PaO2 mmHg for oxygenation

›PaO2 below 60 mmHg is critical threshold

›pH for acid-base status

›Venous blood gas

›pH trend assessment when ABG not immediately available

›CO2 trend for ventilation monitoring

›Lactate

06Diagnostic Tests/dt76

Scoring Systems

›PSP severity classification

›Mild PSP

›Perioral and facial paresthesias only

›Mild GI symptoms

›Onset greater than 1 hour post-ingestion

›Symptoms resolve within hours

›Moderate PSP

›Generalized paresthesias

›Extremity weakness and ataxia

›Dysarthria present

›Onset 30 to 60 minutes post-ingestion

›Severe PSP

›Flaccid paralysis

›Dysphagia and respiratory compromise

›Onset within 30 minutes of ingestion

›Most fatalities occur in this group within 12 hours

›Respiratory monitoring thresholds

›Serial NIF and FVC assessment

›NIF below -25 cmH2O triggers urgent intubation consideration

›FVC below 15 mL/kg triggers urgent intubation consideration

›Count-to-20 breath hold test as bedside surrogate

›Rate of progression best predictor of severity

›More rapid onset correlates with higher toxin dose

›2 to 4 hour window is critical observation period

MRI

›MRI role in PSP evaluation

›Generally not indicated if history consistent with PSP

07Disposition/dispo40

ICU admission criteria

›ICU indications

›Respiratory compromise

›Intubated or impending intubation

›Declining NIF or FVC on serial measurements

›SpO2 declining despite supplemental oxygen

›Progressive neurological deterioration

›Worsening weakness on serial exam

›Dysphagia or dysarthria developing

›Rapid onset within 30 minutes of ingestion

›Cardiac involvement

›AV block greater than first degree

›Bradycardia with hemodynamic instability

›Children with any neurologic symptoms beyond paresthesias

›Higher case-fatality risk

›Lower physiologic reserve

Ward admission criteria

›Observation admission for moderate presentation

›Neurologic symptoms beyond mild perioral paresthesias

›Minimum 24-hour observation recommended

›Critical window for respiratory failure is first 12 hours

›Generalized paresthesias with mild weakness

›Serial respiratory monitoring required

›Inability to maintain oral intake

›IV hydration and antiemetic support

Discharge criteria

›Discharge considerations

›Isolated mild perioral and facial paresthesias only

08Treatment/t65

Airway management

›Airway strategy

›Immediate RSI for airway threat

›Succinylcholine 1.5 mg/kg IV for RSI

›Rocuronium 1.2 mg/kg IV alternative if succinylcholine contraindicated

›Existing flaccid paralysis may modify succinylcholine safety profile

›Pre-oxygenation

›100% oxygen by non-rebreather for 3 minutes

›HFNC during pre-oxygenation in cooperative patient

›Post-intubation ventilation settings

›Volume-controlled ventilation initial mode

›Tidal volume 6 to 8 mL/kg ideal body weight

›PEEP 5 cmH2O starting point

›Extubation readiness

›Recovery of PSP typically begins within 12 to 24 hours

›Mild to moderate cases resolve within 2 to 3 days

›Severe weakness may persist up to 1 week

›Standard weaning parameters apply

›NIF better than -25 cmH2O

›FVC greater than 15 mL/kg

›SpO2 adequate on minimal support

Gastrointestinal decontamination

›Activated charcoal

›Dose 1 g/kg oral, maximum 50 g

›Only if within 1 hour of ingestion

›Airway must be protected before administration

›Evidence is limited for saxitoxin binding

›Contraindications

09Special Populations/sp59

Pregnancy

›Pregnancy-specific considerations

›Aspiration risk elevated

›Delayed gastric emptying in second and third trimester

›Increased intraabdominal pressure

›Higher risk of Mendelson syndrome if aspiration occurs

›Fetal monitoring

›Continuous fetal heart rate monitoring for viable gestation

›Maternal hypoxemia causes fetal hypoxemia

›SpO2 target >= 95% to maintain fetal oxygenation

›Imaging approach

›CT head with fetal shielding when clinically necessary

›Do not withhold necessary imaging

›Ultrasound fetal assessment if maternal hemodynamics unstable

›Treatment modifications

›Ondansetron use in pregnancy accepted in most guidelines

›Activated charcoal use acceptable with airway protected

›Intubation threshold lower given higher aspiration risk

›Obstetric consultation for all pregnant patients

Geriatric

›Older adult considerations

›Higher baseline aspiration risk

›Dysphagia more prevalent in older adults

›Oropharyngeal weakness pre-existing

›Reduced physiologic reserve

›Respiratory muscle weakness baseline

›Lower NIF thresholds for intervention

›Earlier intubation consideration

10Background/b94

Epidemiology

›Global burden

›PSP is the most common and most severe form of shellfish poisoning worldwide

›Hundreds of cases reported annually globally

›Significant underreporting due to misdiagnosis

›Worldwide case-fatality rate approximately 6%

›Higher in developing countries

›Higher in pediatric populations

›Most fatalities occur within 12 hours of ingestion

›Geographic distribution

›Temperate coastal waters most commonly affected

›Alaska, Pacific Northwest, Atlantic coast of North America

›Chile, Philippines, parts of Europe, Portugal, Malaysia

›Cases reported globally in 79 countries

›Seasonal patterns

›Historically associated with warmer months

›Spring and summer peak in Northern Hemisphere

›Harmful algal blooms correlate with warming waters

›Climate change extending bloom seasons

›Year-round risk increasing in some regions

›Recreational harvesting season overlap

›Higher case rates when public self-harvesting increases

›Vector species

›Bivalve mollusks primary vectors

›Clams and mussels most common sources

›Oysters and scallops also implicated

›Non-traditional vectors

›Puffer fish (tetrodotoxin overlap)

›Lobster and xanthid crabs

›Larger specimens may accumulate higher toxin concentrations

Pathophysiology

›Toxin mechanism

›Saxitoxin family of neurotoxins

›More than 50 structurally related saxitoxin congeners identified

›Potency varies among congeners

›Produced by dinoflagellates Alexandrium, Gymnodinium, and Pyrodinium species

›Sodium channel blockade mechanism

›Blocks voltage-gated sodium channels at the channel pore

›Prevents sodium ion influx required for action potential

›Affects peripheral motor nerves, sensory nerves, and cardiac conduction tissue

›Does not cross blood-brain barrier significantly

›Toxin stability

›Heat-stable and cannot be destroyed by cooking, boiling, or freezing

›Resistant to standard food preparation methods including canning and pickling

›Not inactivated by gastric acid

›Clinical correlation with mechanism

›Peripheral sensory nerve blockade

›Paresthesias and numbness as first symptom

›Perioral distribution from early high-concentration exposure

›Peripheral motor nerve blockade

›Flaccid paralysis without upper motor neuron signs

›Respiratory muscle paralysis causes death

›AV node conduction suppression

›PR interval prolongation and AV block

›Bradycardia without compensatory tachycardia

›Preserved central nervous system function

›Toxin does not cross blood-brain barrier effectively

›Consciousness maintained even with complete peripheral paralysis

›Toxin accumulation in shellfish

›Filter feeders concentrate dinoflagellate toxins

›Shellfish themselves are not harmed

›Toxin concentration highest during bloom events

›Regulatory limits

›800 micrograms saxitoxin equivalent per kilogram shellfish meat

›European Union and North American regulatory threshold

Therapeutic Considerations

›No antidote currently available

›Saxitoxin-specific antibodies developed in animal models

›Not available for human clinical use

›Investigational stage only

›All treatment is supportive

›Respiratory support is the life-saving intervention

›Most patients recover fully with adequate ventilatory support

›Recovery timeline

›Mild to moderate cases resolve within 2 to 3 days

›Severe weakness may persist up to 1 week

›No known long-term neurologic sequelae in survivors

›Evidence basis for management

›Supportive care and early intubation for respiratory failure

›Class I recommendation for airway management

›Expert consensus given no antidote available

›Activated charcoal role limited

›ACEP Level C recommendation given limited evidence

›Benefit only if within 1 hour and airway protected

›Poison control consultation improves outcomes

›Coordination of public health response

›Guidance on atypical presentations

›Public health considerations

›Mandatory reporting in most jurisdictions

›Cluster investigation prevents additional cases

›Shellfish source identification and recall

›Monitoring programs

›FDA and state programs monitor commercial shellfish

›Recreational harvesting areas require self-monitoring

›Prevention counseling

›Heed all harvesting bans and red tide advisories

›No preparation method renders contaminated shellfish safe

11Patient Discharge Instructions/pdi28

copy discharge instructions

›What happened

›You were diagnosed with paralytic shellfish poisoning

›A powerful toxin called saxitoxin was in the shellfish you ate

›This toxin blocks nerves temporarily

›There is no antidote and most people recover fully

›At home care

›Rest until all tingling, numbness, and weakness have fully resolved

›Stay well hydrated with clear fluids

›Eat only soft easily chewed foods until swallowing feels completely normal

›Avoid alcohol for at least 48 hours

›Avoid all opioid pain medications and sedatives unless prescribed for another reason

›Return to the emergency department immediately if

›Any difficulty breathing or shortness of breath

›Any difficulty swallowing or speaking

›Worsening numbness or weakness after leaving the hospital

›Feeling faint or losing consciousness

›Irregular or very slow heartbeat

›Symptoms that return after improving

›Shellfish safety instructions

›Do not eat shellfish from the same source that made you ill

›Do not harvest shellfish from any area with a current red tide or bloom advisory

›Cooking, boiling, freezing, or canning does not make contaminated shellfish safe

›Report your illness to your local health department

›Alert anyone else who ate the same meal to seek medical attention if symptomatic

›Follow up

›Family physician or clinic within 1 week

›Sooner if any residual numbness, weakness, or swallowing difficulty

12References/r26

Guidelines and key sources

›Primary references

›CDC Yellow Book 2025 — Ansdell VE, Food Poisoning from Marine Toxins

›Comprehensive review of PSP epidemiology and management

›CDC travel health guidance framework

›Etheridge SM. Paralytic Shellfish Poisoning: Seafood Safety and Human Health Perspectives. Toxicon. 2010

›PubMed PMID 20035780

›Pathophysiology and AV node conduction effects

›Isbister GK, Kiernan MC. Neurotoxic Marine Poisoning. Lancet Neurology. 2005

›PubMed PMID 15778101

›Clinical differentiation of shellfish toxin syndromes

›Additional clinical references

›Acres J, Gray J. Paralytic Shellfish Poisoning. Canadian Medical Association Journal. 1978

›PubMed PMID 570450

›Clinical management framework

›Sobel J, Painter J. Illnesses Caused by Marine Toxins. Clinical Infectious Diseases. 2005

›PubMed PMID 16206104

›Disposition and treatment evidence

›Knaack JS et al. Case Diagnosis and Characterization of Suspected PSP in Alaska. Harmful Algae. 2016

›PubMed PMID 28918891

›Diagnostic characterization and HPLC-MS/MS confirmation

›ICD-10 coding references

›T61.771 — Saxitoxin poisoning (paralytic shellfish poisoning)

›Primary diagnostic code for PSP

›T61.01 — Ciguatera fish poisoning for differential

›A05.1 — Botulism for differential

›G61.0 — Guillain-Barre syndrome for differential

Evidence & Review

Evidence & Review