Pertinent Questioning & Field Differential

History & Onset

• Has this happened before? What happened last time, what was done, does this feel the same?
• Chest pain present? Which came first — CP or SOB?
• Ever been intubated or placed on CPAP before?
• What were you doing when it started? Sudden or gradual onset?
• Acute onset suggests allergic reaction, asthma, or CHF flash pulmonary edema. Gradual onset suggests COPD or evolving MI.

OPQRST

HAM & Delegate

• Monitor / pulse ox / vitals / oxygen
• Pupils? 12-lead? Blood sugar? CVA assessment? Temperature?
• Lung sounds — always

Lung Sounds & Associated Symptoms

• Cough? Sputum — color, blood? (yellow-green = pneumonia; pink frothy = CHF; blood-tinged = PE/trauma)
• Recent illness, fever/chills, runny nose? (pneumonia/cold)
• Recent stress, numbness/tingling around lips or fingers? (hyperventilation/psychological)
• Recent fall or trauma? (pneumothorax)
• Recent strenuous/exertional activity? (asthma)
• Sleep position, pillows, orthopnea? (CHF)
• Recent surgery, long travel, scuba, fracture, pregnancy, cancer, immobilization? (PE)
• Known triggers? (allergic reaction/asthma)
• Last oral intake, allergen exposure, new soap/detergent, new medication, sting/bite? (allergic reaction)
• Smoker? Toxic inhalation possible? Home oxygen? Hx of CHF/COPD/asthma?

Peds-Specific SOB (2nd reference)

• Recent illness / URI? Fever? Runny nose? Cough/sneezing? Tugging at ear?
• Acute or gradual onset? Normal color? Normal behavior?
• Vaccinations up to date? Prior intubation/hospitalization?

Physical Exam / Check

• Vitals (HR, BP, RR, skin, GCS), 12-lead, pupils, blood sugar, CVA assessment, temp, lung sounds
• Wheezes/rhonchi, cyanosis, clipped speech, pursed-lip breathing, accessory muscle use
• Edema, JVD, pink frothy sputum, flushing, urticaria, hives
• Capnography, CPAP, and nasotracheal intubation are on the table as needed

Pathophysiology — Why We Ask

• Dyspnea is a mismatch between respiratory drive and the ability to move air; every question is hunting for where the mismatch lives: pump (heart), airway, gas exchange, or a false alarm (anxiety).
• Orthopnea: lying flat increases venous return/preload; a failing left heart backs that volume into pulmonary capillaries, raising hydrostatic pressure until fluid pushes into alveoli.
• Sudden onset = mechanical/embolic (PE, pneumothorax) or triggered (anaphylaxis — fast mast-cell degranulation). Gradual onset = accumulating process (CHF fluid, pneumonia inflammation, COPD airway narrowing).
• Air in vs. out: inspiratory difficulty → upper airway obstruction (epiglottitis, croup, FBAO). Expiratory difficulty/wheeze → lower airway narrowing (asthma/COPD) — exhalation is passive recoil, and narrowed airways collapse further under forced expiration, trapping air.
• Sputum color: neutrophil-driven yellow-green = bacterial pneumonia; pink frothy = plasma leaking through stressed alveolar-capillary membranes under high hydrostatic pressure (CHF); blood-streaked = airway trauma, PE infarction, or malignancy.
• DVT/immobility risk factors map to Virchow's Triad (stasis, hypercoagulability, endothelial injury) — the embolized clot obstructs perfusion to ventilated alveoli, producing wasted ventilation, hence hypoxic/tachypneic patients with clear lungs.
• Perioral/digital numbness in hyperventilation: blowing off CO2 causes respiratory alkalosis, which shifts free calcium onto albumin, lowering ionized calcium and raising neuromuscular excitability.
• V/Q mismatch is the unifying mechanical concept behind hypoxia in almost every SOB etiology: PE creates dead space (ventilated, not perfused), pneumonia/CHF create shunt (perfused, not ventilated) — both drop PaO2 but respond very differently to supplemental O2 (shunt physiology is classically less O2-responsive than dead-space physiology).
• Accessory muscle use and tripoding reflect the body recruiting the sternocleidomastoids, scalenes, and abdominal muscles once the diaphragm alone can no longer generate adequate tidal volume — a visible marker of impending respiratory fatigue and failure.
• Capnography waveform shape is diagnostic on its own: a rising "shark-fin" phase 3 slope reflects delayed, uneven alveolar emptying from bronchoconstriction (asthma/COPD), while a normal box-shaped waveform with low EtCO2 and high RR fits hyperventilation syndrome.

Diagnostic Testing & Rule-Out Strategy

• Field: SpO2 and waveform capnography (shape distinguishes obstructive disease from normal/hyperventilation patterns), 12-lead ECG (screens cardiac contribution/strain), blood glucose, lung sound auscultation.
• ED-level: CXR (pneumonia infiltrate, CHF vascular congestion/Kerley B lines, pneumothorax), BNP/NT-proBNP (elevated in CHF from ventricular stretch), D-dimer → CT pulmonary angiogram if PE suspected, ABG/VBG for gas exchange and acid-base status, troponin if cardiac ischemia is on the differential.
• Bedside ultrasound (where available): lung ultrasound B-lines support CHF/pulmonary edema; absent lung sliding supports pneumothorax.

Common SOB Calls

• CHF, COPD, Asthma, Pneumonia, Arrhythmia, Allergic Reaction, MI, PE, Anxiety, Pneumothorax

Disease Reference

SAD CHF (Heart)

• Chest pain? CP with CP (crushing chest pain)? Pink frothy sputum?
• DOE — how are you getting around?
• PND? Orthopnea? Pillow count?
• Pedal edema? Crackles/rales on auscultation?

Obstructive

• Stridor? Foreign body airway obstruction?
• Allergic trigger? (including ACE-inhibitor angioedema)
• Infection — croup & epiglottitis?

Reactive

• Asthma or COPD history? Change in cough?
• History of intubation or hospitalization?
• Did they try their inhaler — did it help?
• Past exacerbations — how does this compare?

Infection ("Wind or Water")

• Pneumonia? Fever/chills? Sputum? Body aches?

Death (Can't-Miss Mimics)

• PE or pneumothorax being masked as a routine SOB call?

Pathophysiology — Why We Ask

• SAD CHF pathophysiology mirrors the CHF entry covered under Chest Pain and SOB: failing left-ventricular forward flow backs pressure into the pulmonary circuit, driving fluid across the alveolar-capillary membrane (crackles, frothy sputum), while a failing right ventricle backs pressure into the systemic venous system (JVD, edema, hepatic congestion).
• Obstructive causes (FBAO, angioedema, croup/epiglottitis) share a mechanical narrowing of a fixed-diameter airway — because resistance to flow rises with the fourth power of a shrinking radius (Poiseuille's law), even modest additional swelling on an already-narrow pediatric or edematous airway causes a disproportionate jump in work of breathing.
• Reactive airway disease (asthma/COPD) involves bronchial smooth muscle constriction, mucosal edema, and mucus plugging — three separate mechanisms, which is why a single medication class may not fully reverse an exacerbation.

Diagnostic Testing & Rule-Out Strategy

• Field: lung auscultation for crackles vs. wheeze, SpO2/EtCO2, 12-lead for strain pattern or arrhythmia, response to a trial of bronchodilator (reactive) or CPAP/nitro (CHF) can itself be diagnostic.
• ED-level: CXR, BNP, ABG, and for suspected foreign body or epiglottitis, direct/indirect airway visualization (often deferred until a controlled airway setting given risk of complete obstruction with agitation).

History

• Has this happened before? What happened last time, what was done, does this feel the same?

OPQRST

HAM & Delegate

• Monitor / pulse ox / vitals / oxygen / 12-lead + lung sounds
• Pupils? Blood sugar? Temp?
• Orthostatic vitals

GI / Constitutional

• Pain radiating to the back? (AAA)
• N/V — keeping anything down? (bowel obstruction)
• Blood or coffee grounds in vomit — color, amount? (TACO: color, amount, consistency, onset)
• Which came first, pain or vomiting? (pain-first is more concerning)
• Last bowel movement, regular? Blood/tarry stools — bright vs. dark? Consistency — hard or diarrhea?
• Urinating regularly, last time, pain/burning? Color, blood, cloudy, foul smell, frequency? (UTI/kidney stones/PID)
• Recent illness? Dizzy or lightheaded?
• Drug/alcohol abuse, chewing tobacco? (liver disease/cirrhosis)
• Recent falls or heavy lifting? (hernia/testicular torsion/hemorrhoids)
• History of ulcers? Still have gallbladder/appendix? History of kidney stones or gallstones?
• Last oral intake — fatty, greasy, spicy? Any diet changes?

Females

• Chance of pregnancy? Last menstrual period, normal?
• Flow normal? Abnormal discharge, color? Pad count in last 24 hours (1 pad ≈ 30cc)
• Sexually active? Pain with intercourse? Pelvic pain? (PID)

Physical Exam / Check

• Inspect/palpate abdomen, orthostatics, CVA assessment
• Guarding, bloating, rigidity, pinpoint tenderness, rebound tenderness, pulsating masses, soft & supple?

Pathophysiology — Why We Ask

• Visceral pain (poorly localized, dull, crampy) fires along autonomic afferents shared across several dermatomes. Somatic/parietal pain (sharp, localized, worse with movement) fires once inflammation reaches the somatically-innervated parietal peritoneum — that shift is the tell that a process has become surgical.
• Constant vs. intermittent: colicky pain = a hollow organ contracting against an obstruction (bowel, biliary, ureteral). Constant pain = ischemia, inflammation, or perforation — none of which resolve with peristalsis.
• Radiation: gallbladder to right shoulder, spleen to left shoulder, kidney to flank — referred pain follows shared embryologic/dermatomal wiring between the organ and that somatic region.
• Timing of vomiting vs. pain: in appendicitis, pain classically precedes vomiting (vagal reflex from visceral distension). Vomiting-first suggests gastroenteritis (an irritant/toxin process).
• Melena vs. hematochezia: blood altered by gastric acid/gut transit turns black and tarry (melena = upper GI, above the ligament of Treitz). Bright red blood hasn't been digested (lower GI, or a fast massive upper bleed).
• Fatty-food trigger: CCK release after a fatty meal makes the gallbladder contract against an obstructing stone — explains the classic 30–60 minute post-meal cholecystitis pain.
• AAA/pulsatile mass + back pain: the aorta shares embryologic/retroperitoneal proximity; a leaking or expanding aneurysm irritates retroperitoneal structures producing the classic tearing back pain, and the palpable pulsatile mass is the dilated vessel wall itself.
• Rebound tenderness occurs because releasing pressure lets the inflamed peritoneum snap back and stretch rapidly, firing more nociceptors than steady palpation does — it is a more specific (though less sensitive) sign of peritonitis than tenderness alone.
• Rovsing's, psoas, and obturator signs (indirect peritoneal irritation tests) work by stretching or compressing an inflamed structure indirectly — a retrocecal appendix, for example, may not be tender on direct palpation but will be positive on psoas sign because the inflamed appendix lies against the psoas muscle.
• Orthostatic vital sign changes reflect intravascular volume status — a significant heart rate rise or BP drop on standing suggests the patient has already lost a meaningful fraction of circulating volume (bleeding, dehydration, third-spacing) even while supine vitals still look reassuring.

Diagnostic Testing & Rule-Out Strategy

• Field: orthostatic vitals, blood glucose, 12-lead (atypical MI can present as epigastric pain, especially inferior wall MI).
• ED-level: CBC (leukocytosis, anemia from bleeding), lipase/amylase (pancreatitis), liver panel (hepatobiliary source), lactate (mesenteric ischemia, sepsis), urinalysis (UTI/stones), beta-hCG in any female of childbearing age (mandatory before imaging with radiation and before certain medications), CT abdomen/pelvis with contrast for most acute abdomens, RUQ ultrasound specifically for gallbladder pathology, bedside FAST exam if trauma-associated or hemodynamically unstable to screen for free fluid.

Radiation Key

• Radiates to right shoulder = gallbladder · Radiates to left shoulder = spleen · Radiates to flank = kidney
• Visceral: intermittent, dull, cramping, moving, not localized · Somatic: constant, sharp, aggravated by movement, localized
• Upper GI: bleeding above the ligament of Treitz (duodenum) · Lower GI: bleeding distal to the ligament

Disease Reference

Immediate Field Assessment

• Check for crowning?
• How far apart are the contractions?
• Delegate: monitor / pulse ox / vitals / oxygen + pupils / 12-lead / blood sugar / CVA assessment / temp / lung sounds

Abdominal / Contraction Pain (OPQRST)

• Perform full abdominal assessment along with OPQRST

PALB — Current Pregnancy

Current Pregnancy Detail (2nd reference)

• Weeks of gestation? Expected delivery date? Prenatal care?
• Multiple fetuses? Abnormal fetal positioning?
• False labor symptoms? Consider eclampsia.

Previous Pregnancies

• Gravida / Para?
• Was the last pregnancy normal?
• Miscarriages? Abortions? C-sections?

HAM & Risk Screen

• High-risk pregnancy? Problems with this or prior pregnancies?
• Abnormal discharge? Bleeding/spotting — how fast filling pads? (menorrhagia)
• Frequent urination, headache, high BP? (pre-eclampsia)
• Substance use? Recent injury or trauma? (abruptio placenta)
• Hypertension — old or new? Diabetes? Drugs/alcohol during pregnancy?

Physical Exam

• Last menstrual period, normal/light/heavy flow?
• Pad count in last 24 hours?
• Chance of pregnancy? Sexually active? Pelvic pain? Foul-smelling urine? (PID) Pain with urination? (UTI)

Trimester & Labor Reference

• 1st Trimester: 1–12 weeks (1–3 months) · 2nd: 13–27 weeks (4–6 months) · 3rd: 28–40 weeks (7–9 months) · Full term: 37–42 weeks from LMP
• 1st Stage of Labor: blood show/bag of waters, dilates to 10cm, contractions >5min lasting 1min
• 2nd Stage of Labor: cervix fully dilated, crowning, birth of baby
• 3rd Stage of Labor: birth of placenta

Disease Reference

Pathophysiology — Why We Ask

• Every question funnels toward one operational decision: deliver in the field, or transport? Contraction frequency/duration, urge to push, and rupture of membranes are the direct inputs to that call.
• BP + headache + vision changes screens pre-eclampsia → eclampsia: vasospasm and endothelial dysfunction raise BP and can precipitate seizures, a life threat to mother and fetus.
• Bleeding character separates two very different 3rd-trimester emergencies: abruption (painful, dark, firm uterus — the placenta is tearing away, concealing blood behind it) vs. previa (painless, bright red — the placenta itself is the bleeding source over the cervix). Digital exam is contraindicated in either until previa is ruled out.
• Uterine tone on palpation is a direct physical proxy for concealed hemorrhage: a soft, non-tender uterus in a bleeding patient favors previa (bleeding is external and visible), while a firm, board-like, painful uterus favors abruption (blood is trapped between the placenta and uterine wall, distending it internally even though external bleeding may look minimal).
• Supine hypotensive syndrome in the third trimester happens because the gravid uterus compresses the inferior vena cava when the mother lies flat, reducing venous return and cardiac output — this is why late-pregnancy patients are transported tilted left, not supine.

Diagnostic Testing & Rule-Out Strategy

• Field: fundal height/contraction timing by palpation, FHR if equipment available, visual inspection for crowning/bleeding/prolapse, BP for pre-eclampsia screening.
• ED-level: beta-hCG and quantitative trend (for suspected ectopic), transvaginal/transabdominal ultrasound (locates the pregnancy, assesses viability, evaluates for abruption/previa), CBC and type & screen (anticipating possible transfusion need), urine protein (pre-eclampsia), continuous fetal monitoring (tocometry + FHR) once at a receiving facility.

History

• Happened before? What happened last time, does this feel the same?
• SOB present — which came first, CP or SOB?
• Prior heart attack — does this feel like that one?

OPQRST

HAM & Delegate

• Monitor / pulse ox / 12-lead / vitals / oxygen
• Blood sugar? Pupils? Lung sounds? Temp?

R/O PAPPA — Associated Symptoms (2nd reference)

• How is breathing — primary or secondary to the CP? Difficulty breathing before or after the CP began?
• Pain on inspiration, palpation, or movement?
• N/V? Sudden sweats? Swelling? Weakness or dizziness?
• Recent injury or illness? Fever/chills?
• Cough — productive, color, painful? Pain/tenderness to the calf? (DVT/PE screen)

Detailed Symptom Screen

• N/V — blood or coffee grounds in vomit? (MI/AAA/aortic dissection)
• Headache, blurred vision, ringing in ears? (HTN/CHF/MI)
• Dizzy or passed out — how long, witnessed? Head/neck/back pain? (MI/AAA/aortic dissection)
• Recent illness or fever? (pneumonia) Recent cough, sputum color, blood? (CHF/pneumonia)
• Recent trauma or falls? (trauma/AAA/aortic dissection)
• Recent strenuous activity or stress? (MI risk)
• History of anxiety? Numbness/tingling in fingers or around the mouth? (hyperventilation/anxiety)
• Back/abdominal pain? Pulsating masses? (aortic dissection/AAA) — palpate abdomen
• Last oral intake — alcohol/drugs/caffeine? (GERD/MI risk)
• History of indigestion? Spicy/fatty foods recently? Feels like indigestion? (GERD)
• Starts after a meal? History of gallstones?
• Recent surgery, fractures, long travel, scuba, pregnancy? (PE)
• Need extra pillows to sleep? SOB lying supine? (orthopnea/PND — CHF)
• Chest tightness? (allergic reaction, anxiety, asthma, pneumonia, COPD, heavy coughing)
• Family hx? Smoker? Diabetic? Overweight? HTN? Kidney disease? (CAD risk factors)

Physical Exam / Check

• Vitals (HR, BP, RR, skin, GCS), 12-lead, pupils, blood sugar, lung sounds, temp, orthostatics

Pathophysiology — Why We Ask

• Myocardial ischemia = oxygen supply failing to meet demand (HR × wall tension × contractility). Cardiac pain is visceral, carried by sympathetic afferents entering at T1–T4, which is why it's diffuse, pressure-like, and refers to the arm/jaw.
• Reproducible on palpation suggests a musculoskeletal source (costochondritis) — you're directly stimulating somatic fibers. True cardiac pain, being visceral, isn't affected by external palpation. Useful but not absolute.
• Pleuritic pain (worse with breathing) means the somatically-innervated parietal pleura is irritated — PE infarction, pneumothorax, pericarditis extending to the pleura, or pneumonia. Cardiac ischemic pain is not pleuritic.
• Better leaning forward = pericarditis: the inflamed parietal pericardium contacts the heart when supine, and leaning forward pulls the heart away from it, reducing friction.
• Tearing pain radiating to the back = aortic dissection: a torn intima lets blood dissect between the aortic wall layers, tracking posteriorly along the vessel and irritating perivascular structures the whole length of the tear — mechanically different from the referred pain of MI.
• Unequal arm BPs reflect a dissection flap differentially compromising subclavian flow depending on where the false lumen propagates.
• ST elevation reflects a transmural injury current (the injured wall can't fully repolarize, creating a voltage gradient). ST depression reflects subendocardial ischemia — the innermost layer is furthest from epicardial coronary vessels and under the highest wall tension, making it most vulnerable.
• Risk factors (DM, HTN, smoking) accelerate atherosclerosis — endothelial injury, lipid deposition, plaque formation, eventual rupture and thrombus — raising pre-test probability when the 12-lead is equivocal.
• Troponin kinetics explain why a single negative troponin doesn't rule out MI in the field or immediately in the ED: troponin is released as myocytes become necrotic, which takes hours to become detectable after the ischemic insult begins — serial troponins over time, not one value, define the rule-out.
• Kussmaul's sign and pulsus paradoxus in tamponade reflect the same physiology from two angles: fluid in a non-compliant pericardial sac limits diastolic filling, so inspiration (which normally increases right heart filling) instead pulls the interventricular septum toward the underfilled left ventricle, dropping stroke volume and systolic pressure with each breath.

Diagnostic Testing & Rule-Out Strategy

• Field: 12-lead ECG (the single highest-yield prehospital test — look for STEMI criteria, reciprocal changes, right-sided leads for RVI), SpO2, blood pressure in both arms if dissection is suspected, lung sounds.
• ED-level: serial troponin (kinetics matter more than a single value), CXR (widened mediastinum in dissection, infiltrate in pneumonia, pneumothorax), D-dimer → CTA chest for PE, CT angiogram of the chest/aorta for suspected dissection, bedside echo for tamponade/wall motion abnormality, lipase if epigastric overlap with pancreatitis is possible.

Common Chest Pain Calls

• MI, Arrhythmia, SVT, PE, Trauma, Allergic Reaction, Pericarditis, Pleurisy, Anxiety, GERD, CHF, Asthma, Pneumonia, AAA

ECG Reference

• Elevation = injury · Depression = ischemia · Q waves = infarction (1mm)
• ST elevation imitators: BBB, ventricular rhythms, LVH, benign early repolarization (BER), paced rhythms
• SALI — Septal, Anterior, Lateral, Inferior
• RVI: II, III, aVF; run R-sided 12-lead; CP, hypotension, bradycardia, edema, JVD → O2/Aspirin/Fluids/Morphine, 0 Nitro
• LVI: V1–V6, I, aVL; CP, pulmonary edema, SOB, tachycardia, diaphoresis → O2/Aspirin/Nitro/Morphine, 0 Fluids

Disease Reference

Accessory Pathways (Preexcitation)

• Wolff-Parkinson-White: slurred QRS (delta wave); accessory pathway may reach the conduction system first, causing PSVT
• Lown-Ganong-Levine: shortened PR interval capable of producing PSVT; slurred QRS usually not seen

General Screen

• Age? Weight?
• How does the child normally act? Normal mentation?
• Did they stop breathing at all — how long? (ALTE)
• Did they change color?
• Recent sickness — how long, fever? (infection)
• Recent trauma?

HAM & Delegate

• Monitor / pulse ox / vitals / oxygen + pupils / 12-lead / blood sugar / temp / lung sounds
• (Consider asthma as a driver of respiratory presentation)

Feeding & Output

• Vomiting/diarrhea — how long, how much, color, blood? (dehydration)
• Eating/drinking regularly — last time, what, how much, is that normal?
• Diaper count in last 24 hours — is that normal?
• What were they doing prior to the incident?
• Cry sound normal?
• Taking regular naps? Lethargic?
• Seizure activity? Body temperature?
• Cough, sputum, color, lung sounds?
• Full term birth? Pregnancy complications? Prenatal care? Last doctor visit?

Physical Exam

• Toe-to-head exam
• AEIOU-TIPS for AMS
• Objective findings: bulging/sunken fontanels, skin turgor, retractions

Category Reference

• All peds calls fall under: Respiratory, Environmental, Congenital, Trauma, Dehydration

Pediatric Vital Signs

• Newborn: RR 30–60, HR 100–160, Systolic >60
• Infant: RR 20–30, HR 100–160, Systolic >60
• Toddler (1–3): RR 20–40, HR 90–150, Systolic >70
• Preschooler (3–6): RR 22–34, HR 80–140, Systolic >75
• School Age (6–12): RR 18–30, HR 70–120, Systolic >80
• Adolescent (13+): RR 12–20, HR 60–100, Systolic >90

Neonatal Resuscitation (APGAR at 1 & 5 min)

• Warm/dry/stimulate → breathing/crying/good tone: give to mom, provide warmth, clear airway, dry, ongoing eval
• HR <100? Gasping or apnea? → PPV/SpO2, clear airway
• After 60 sec, HR still <100? → take ventilation corrective steps
• HR <60? → start compressions with PPV, consider intubation
• HR still <60? → IV epinephrine

Pathophysiology — Why We Ask

• Children compensate for physiologic stress remarkably well and then decompensate suddenly — their stroke volume is relatively fixed, so cardiac output depends almost entirely on heart rate, meaning tachycardia is often the earliest and sometimes only sign of shock long before blood pressure drops.
• Feeding and urine output are used as dehydration proxies because children have a higher body-surface-area-to-volume ratio and higher baseline metabolic/fluid turnover than adults — they dehydrate faster and have less physiologic reserve to buffer losses.
• Fontanelles are a direct, non-invasive window into intracranial pressure in infants before the skull sutures fuse — a bulging fontanelle suggests elevated ICP (meningitis, hydrocephalus, hemorrhage), while a sunken fontanelle suggests significant dehydration.

Diagnostic Testing & Rule-Out Strategy

• Field: weight-based vital sign comparison against age norms, blood glucose, capillary refill and skin turgor as rapid dehydration/perfusion proxies, temperature.
• ED-level: CBC and blood cultures if sepsis is suspected, urinalysis (common occult infection source in young febrile children), viral respiratory panel, CXR for respiratory presentations, lumbar puncture if meningitis is suspected (bulging fontanelle, nuchal rigidity, ill-appearing febrile infant).

Disease Reference

Key Additions Beyond Standard Seizure Workup

• Fever present? Medications given to break the fever?
• Diaper output — urine, vomit, stool?
• Did they get into anything (ingestion)?
• Vaccinations up to date?
• Normal childbirth? Consider ALTE?

Pathophysiology — Why We Ask

• The rate of temperature rise, not the absolute peak, is thought to trigger febrile seizures — rapidly increasing core temperature transiently lowers the seizure threshold in the immature pediatric cortex, which is why they often occur early in a febrile illness rather than at the fever's peak.

Diagnostic Testing & Rule-Out Strategy

• Field: blood glucose (mandatory in every seizure), temperature, thorough history for a simple vs. complex febrile seizure pattern.
• ED-level: typically minimal further workup for a classic simple febrile seizure with a clear source of fever and rapid return to baseline; blood glucose, electrolytes, and further neuroimaging/LP are reserved for atypical features (age <6 months or >5 years, focal findings, prolonged postictal state, no clear fever source, or a first complex febrile seizure).

Pathophysiology — Why We Ask

• Febrile seizures occur from the rapid rate of temperature rise more than the absolute peak temperature — the immature pediatric brain is more susceptible to seizure from fever than an adult brain.
• Ingestion screening matters because toddlers explore by mouth; many common household substances (and some medications) lower seizure threshold or are directly neurotoxic.

Scene & History

• C-spine? Fall or assisted to the ground?
• Happened before? What happened last time, any deficits remaining from a prior stroke?
• Last time seen acting normal?
• Complaining of anything before this — N/V, dizziness, headache, CP, tingling/numbness?

HAM & Delegate

• Monitor / pulse ox / vitals / oxygen / pupils / blood sugar / 12-lead / temp / lung sounds

GCS / LOC

• What is your name? Where are you right now? What day of the week is it? Who is our president?
• OPQRST if positive LOC

Stroke Scale Exam

• Smile (facial symmetry), grips/arm drift, pushes/pulls (feet), slurred speech?
• Check pupils, blood sugar, 12-lead
• Trouble swallowing? Pain? Dizziness? Blurred vision? Ringing in ears/hearing loss? Nosebleeds? N/V?

Onset & Risk Screen

• Sudden or gradual onset?
• Headache? Blurred vision? Ringing in ears? (HTN/hemorrhagic)
• Recent fall, trauma, or surgery?
• New-onset seizure? History of seizures or epilepsy?
• History of diabetes? History of HTN?
• A-fib? History of clots/DVT? Smoker? Drug use (cocaine)?
• Medication reaction? Dystonic reaction?
• Sick recently? Fever/chills?
• Old neurological deficits for comparison?
• TIME OF ONSET — the single most important data point.

mLAPSS Screen

• Last seen normal or without stroke symptoms?
• No history of seizures or epilepsy
• Age ≥40 (if <40, continue mLAPSS)
• Not wheelchair-bound or bedridden
• BGL between 60–400 mg/dL
• 1 positive motor finding: facial smile/grimace asymmetry, grip asymmetry, arm strength asymmetry

Thrombolytic Assessment

• Onset >4 hours ago?
• History of recent bleeding? Anticoagulant use?
• Major surgery or serious trauma in the previous 14 days?
• Sustained systolic BP >185?
• Recent CVA or intracranial hemorrhage?

Physical Exam

• Speech impairment, aphasia, dysphasia, ALOC, paresthesias, new-onset seizures, dizziness, one-sided weakness, visual disturbances, HTN, headache/blurred vision/tinnitus, N/V
• Contact NSRC base station
• Treatment: C-spine, O2, IV lock, treat seizure/hypoglycemia, transport to appropriate facility

San Bernardino County Decision Tree

• >8 hours or unknown = closest paramedic receiving hospital
• 3–8 hours = NSRC-I
• <3 hours = any closest NSRC I or NSRC II

Pathophysiology — Why We Ask

• Brain tissue has essentially no glucose/O2 reserve — infarction begins within minutes of vessel occlusion. Every question is chasing one thing: how much salvageable penumbra is left, and is there still time to act?
• Last known normal matters because thrombolytics dissolve clot to reperfuse the penumbra (ischemic but not-yet-dead tissue). Past the window, reperfusing already-dead tissue causes hemorrhagic transformation instead of benefit — a hard biological cutoff, not an arbitrary rule.
• Facial droop/arm drift/slurred speech map to the corticospinal tract; unilateral weakness reflects a contralateral lesion, since each hemisphere controls the opposite body side.
• Territory-specific findings reflect which vascular bed is starved — MCA (aphasia, hemiparesis face+arm>leg), ACA (leg-predominant), PCA (visual field deficit) — essentially vascular anatomy mapped onto function.
• Excluding seizure history matters because postictal (Todd's) paralysis is a stroke-mimic from neuronal exhaustion, not vascular occlusion, and it resolves.
• Glucose 60–400 requirement exists because both hypo- and hyperglycemia can cause focal deficits that mimic stroke — hypoglycemic hemiparesis is real and documented.
• Hemorrhagic vs. ischemic: hemorrhagic strokes present with more severe headache and higher BP because the mechanism is a ruptured vessel (often from chronic-HTN microaneurysms), not a gradual occlusive process.
• The ischemic core vs. penumbra concept underlies every stroke scale: the core is already dead, but the penumbra is hypoperfused, electrically silent, yet still metabolically viable tissue kept alive by collateral flow — time-dependent treatment exists purely to rescue that penumbra before collaterals fail too.
• Blood pressure management differs by stroke type because the physiology is opposite: in ischemic stroke, elevated BP may be a compensatory mechanism preserving penumbral perfusion (permissive hypertension pre-thrombolysis), while in hemorrhagic stroke, elevated BP actively drives ongoing bleeding and hematoma expansion.

Diagnostic Testing & Rule-Out Strategy

• Field: blood glucose (mandatory before any stroke scale is trusted), stroke scale exam, exact time of onset/last known normal, 12-lead (screens for A-fib as a source and for concurrent cardiac events).
• ED-level: non-contrast head CT first (primary goal: rule out hemorrhage before any thrombolytic can be given), CT angiogram to identify a large-vessel occlusion for possible thrombectomy candidacy, CT perfusion or MRI to estimate salvageable penumbra in extended time windows, coagulation studies if on anticoagulants, glucose and electrolytes to exclude metabolic stroke mimics.

Territory Reference

• Hemorrhagic Strokes: significant HTN, sudden onset
• Ischemic Strokes: embolic (clot travels from elsewhere) or thrombotic (develops in place)
• Middle Cerebral Artery: aphasia, neglect, hemiparesis, gaze deviation toward the affected side
• Anterior Cerebral Artery: hemiparesis of the leg
• Posterior Cerebral Artery: visual field deficit
• Basilar Artery: coma, gaze abnormality, vertigo, respiratory changes
• Small Vessel: pure motor symptoms to face, arm, and leg of one side

History

• History of trauma?
• New or old history — how often do you get these? How does this one compare?
• N/V? Visual problems, blurred vision? Hearing problems, ringing?
• On blood thinners? History of A-fib?
• Fever/chills/stiff neck?

Exam

• FAST – neuro exam

Pathophysiology / Differential

• Vascular Headache (Migraine): severe pain on one or both sides of the head, from vasodilation/vasospasm and trigeminovascular activation.
• Tension Headache: muscle tension in the face and neck musculature.
• Traction/Inflammatory: secondary to another disorder — CVA, sinus infection, or inflammatory disease.
• Meningitis/Encephalitis: sudden fever, headache, stiff neck, vomiting, confusion, irritability, seizures, LOC — inflammation of the meninges/brain causing raised ICP and meningeal irritation (nuchal rigidity).
• A headache that is the "worst of my life," sudden/thunderclap onset, or accompanied by fever and stiff neck, is treated as a possible subarachnoid hemorrhage or meningitis until proven otherwise — this is why "how does this compare to your usual" is the pivotal question.
• Subarachnoid hemorrhage classically produces a thunderclap headache because blood suddenly irritates meningeal pain fibers and raises intracranial pressure abruptly — unlike the gradual crescendo of a migraine, pain in SAH is typically maximal within seconds.
• Meningeal irritation signs (nuchal rigidity, Brudzinski's, Kernig's) occur because inflamed or blood-irritated meninges cause reflexive muscle spasm when the dura is stretched by neck flexion or leg extension — the body's way of minimizing further stretch of irritated tissue.

Diagnostic Testing & Rule-Out Strategy

• Field: full neuro exam and pupil check, blood pressure (severe hypertension can both cause and result from intracranial pathology), temperature and neck exam for meningismus.
• ED-level: non-contrast head CT (first-line for suspected SAH, especially within the first 6 hours of onset when sensitivity is highest), lumbar puncture if CT is negative but suspicion for SAH remains (looking for xanthochromia), CBC and inflammatory markers if meningitis is suspected, CT angiogram if a vascular cause (aneurysm, dissection) is being considered.

Rule Out

• Arrhythmias, GI bleeds, neuro emergency, hypovolemia

Assessment

• D-stick / 12-lead / neuro exam
• What does the dizziness actually feel like? (room spinning = vertigo vs. presyncope vs. disequilibrium)
• Pain? N/V/D, blood? Vision blurry? Hearing problems?
• Sick recently — fever/chills?
• Stress/caffeine/alcohol use?
• On dialysis? (hyperkalemia risk)
• Skin turgor? Fluid intake?

Pathophysiology — Why We Ask

• "Dizziness" is a symptom umbrella covering true vertigo (vestibular — inner ear or brainstem), presyncope (global cerebral hypoperfusion — cardiac or volume-related), and disequilibrium (proprioceptive/cerebellar). Getting the patient to describe the sensation in their own words is the fastest way to sort the bucket.
• Dialysis/hyperkalemia: missed dialysis allows potassium to accumulate, altering cardiac and neuromuscular membrane potentials — can cause dizziness from dysrhythmia as well as generalized weakness.
• Skin turgor/fluid intake screens for hypovolemia as a presyncope driver — reduced circulating volume drops cerebral perfusion pressure on minimal provocation.
• Orthostatic vs. positional distinction matters mechanistically: orthostatic symptoms track with position change (standing) regardless of head position, driven by blood pressure regulation; true positional vertigo (like BPPV) tracks with head/neck rotation specifically, driven by displaced otoconia in the semicircular canals.
• Central vs. peripheral vertigo is distinguished partly by associated findings — peripheral (inner ear) vertigo is usually severe but isolated, while central (brainstem/cerebellar) vertigo more often comes with other neurologic deficits, because the brainstem houses vestibular nuclei alongside cranial nerve and long-tract pathways in close proximity.

Diagnostic Testing & Rule-Out Strategy

• Field: orthostatic vitals, blood glucose, 12-lead for arrhythmia, focused neuro/cerebellar exam (gait, finger-to-nose, nystagmus pattern) to help separate peripheral from central causes.
• ED-level: CBC (anemia/GI bleed), electrolytes and renal function (especially in dialysis patients), CT or MRI brain if central vertigo is suspected based on exam findings, ECG/telemetry monitoring for intermittent arrhythmia, bedside HINTS exam (head impulse, nystagmus, test of skew) performed by trained clinicians to help differentiate peripheral vertigo from a posterior circulation stroke.

Scene & History

• C-spine? Fall or assisted to the ground? Head/neck/back pain?
• History of seizures? (if no history, perform a CVA assessment instead)
• Witnessed? How long did the seizure last?
• Describe the seizure — full body movement?
• Actively seizing? Apneic?
• Oral trauma? Incontinence?
• History of status epilepticus?

HAM & Delegate

• Monitor / pulse ox / vitals / oxygen / blood sugar / pupils / 12-lead / temp / lung sounds

Medication & Compliance

• Taking medications appropriately? When last taken?
• Recent medication changes? New medications?
• How long on this same dose?
• Recent falls or trauma?
• Recent sickness, N/V (can't keep meds down)?
• Recent drug or alcohol use? (synergistic effect)

Additional Screening (2nd reference)

• Anything different about this seizure compared to prior ones?
• How many seizures — did they regain LOC between them, for how long?
• When was the last seizure?
• Sick recently? Head injury? Drugs/alcohol?
• Full neuro exam
• Can they normally tell a seizure is coming — do they get an aura?

Physical Exam / Check

• Pupils, blood sugar, CVA assessment
• Seizure activity, aura, incontinence, oral trauma
• Treatment: C-spine, O2, IV lock, versed, treat hypoglycemia, CVA assessment

Common Causes

• Drugs, alcohol, medication non-compliance, CNS tumor, stroke, brain bleed, head trauma, hypoglycemia, febrile (peds), epilepsy, hypoxia, electrolyte imbalances, infection/sepsis, HTN

Common Seizure Medications

• Phenytoin (Dilantin), Carbamazepine (Tegretol), Phenobarbital (Luminal), Vigabatrin, Lamotrigine, Gabapentin

Seizure Type Reference

• Generalized: both hemispheres involved (grand mal, absence, tonic, clonic and myoclonic, atonic, infantile spasms)
• Partial: originates in one or more localized foci (simple partial, complex partial, partial with secondary generalization)
• Status Epilepticus: continuous seizure >5 minutes, or two or more seizures without an intervening recovery period
• Absence: seen in childhood — loss of interaction, staring off into space, returns to normal with no memory of the event
• Grand Mal: tonic-clonic — aura, tonic phase (15–30 sec), tonic-clonic phase, postictal state
• Partial: does not impair normal consciousness; can produce bizarre behavior mimicking a psychiatric disorder

Pathophysiology — Why We Ask

• Anti-epileptics stabilize neuronal membranes/enhance GABA inhibition. Subtherapeutic levels from missed doses remove that stabilization and drop the seizure threshold — the single most common reason a known epileptic breaks through.
• Full-body vs. focal semiology tells you where in the brain the abnormal focus lives — generalized seizures involve both hemispheres via thalamocortical circuits from onset; focal seizures originate in one cortical area and may or may not spread.
• Postictal confusion reflects real metabolic exhaustion — spent ATP and accumulated potassium/lactate in the involved neurons — not "faking."
• Incontinence/oral trauma are objective evidence the tonic-clonic motor phase and sphincter loss actually occurred — useful to confirm an unwitnessed event was truly a seizure and not syncope or a psychogenic event.
• Glucose check matters because neurons run almost exclusively on glucose; severe hypoglycemia can itself trigger seizure activity — a fully reversible cause.
• The ictal-postictal cycle reflects a wave of excessive excitatory neurotransmission (often glutamate-driven) followed by a compensatory inhibitory/refractory period once local energy stores (ATP, glucose) are depleted and inhibitory GABA circuits rebound — this is the physiologic basis of the postictal state, not merely "tiredness."
• Status epilepticus becomes progressively harder to terminate the longer it continues because ongoing seizure activity causes internalization of inhibitory GABA-A receptors from the neuronal membrane, effectively removing the brain's own braking mechanism over time — the pharmacologic rationale for early, aggressive benzodiazepine dosing.

Diagnostic Testing & Rule-Out Strategy

• Field: blood glucose (mandatory), temperature, oxygen saturation, thorough witness history of seizure semiology and duration.
• ED-level: anti-epileptic drug levels if the patient is on a known regimen, electrolytes (sodium, calcium, magnesium), toxicology screen, CT head for new-onset seizures or focal findings, EEG for ongoing/subtle status epilepticus or diagnostic classification, lumbar puncture if infection is a concern.

Scene & History

• C-spine? Fall or assisted to the ground? Head/neck/back pain?
• Happened before? What was done last time?
• History of diabetes? Insulin on a regular basis — Type I or II?
• Last insulin dose — when, how much (units), is that the normal amount?
• Taken with a meal? Last time they ate, what did they eat?
• Taking more insulin than normal or standard dose? Last known blood sugar?

HAM & Delegate

• Monitor / pulse ox / vitals / oxygen / blood sugar + pupils / 12-lead / temp / lung sounds

Symptom Screen

• Other medications taken appropriately? Vomiting/unable to keep meds down?
• Pain anywhere? (abdominal pain with high blood sugar)
• Urinating more than normal? (polyuria) Increased thirst? (polydipsia) Increased hunger? (polyphagia)
• Last saw a doctor? Recent illness or trauma?
• Recent stress or strenuous exercise? Recent alcohol or drugs?
• Numbness or tingling to fingers or mouth?

Physical Exam / Check

• CVA assessment, pupils, blood sugar, acetone odor, dehydration/poor skin turgor

Diabetic Medications

• Insulin, Metformin, Acarbose, Miglitol, Saxagliptin, Sitagliptin, Vildagliptin, Glyburide, Glipizide, Glimepiride, Rosiglitazone, Pioglitazone, Colesevelam, Exenatide, Liraglutide, Pramlintide

Blood Glucose Reference

• Normal: 60–120
• Hypoglycemia: ALOC, anxiety, diaphoresis, pale/cool skin, tachycardia/bradycardia, hypotension, nausea, perioral tingling, slurred speech, headache, dizziness, tremors, seizures, impaired vision, hunger
• Hyperglycemia: 3 P's, visual difficulties, fatigue, weight loss, non-healing wounds, dry mouth, dry/itchy skin
• Three P's: Polyuria, Polydipsia, Polyphagia

Electrolyte Quick Reference

• Calcium: cell function, neural transmission, membrane stability, bone structure, coagulation. Hypercalcemia — shortened QT, heart blocks, bradycardia, HTN, polyuria, lethargy
• Potassium: regulates smooth/skeletal/cardiac muscle activity, digestive enzyme reactions, metabolism. Hyperkalemia — peaked T waves, depressed ST segment, depressed P waves, widened QRS, heart blocks, bradycardia
• Sodium: water follows sodium; regulates fluid balance
• Magnesium: regulates calcium absorption and myocardial function, relaxes smooth muscle. Hypermagnesemia — widened QRS, T-wave segment elevation
• Blood pH: 7.35–7.45

Pathophysiology — Why We Ask

• Insulin (from pancreatic beta cells) is the key that lets glucose into cells; without it, glucose stays in the blood while cells starve.
• Insulin timing vs. meal timing: insulin given without adequate carb intake keeps pulling glucose into cells with none replaced from the gut — a straightforward supply/demand mismatch producing hypoglycemia.
• 3 P's: high serum glucose exceeds the kidney's reabsorption threshold, spilling into urine and dragging water osmotically (polyuria) → dehydration → thirst (polydipsia). Meanwhile cells can't access glucose despite high blood levels, so the body signals hunger (polyphagia) — "starving in the midst of plenty."
• Acetone breath/Kussmaul respirations (DKA): without insulin, cells burn fat for energy, producing ketone bodies. Ketones are acidic → metabolic acidosis. Kussmaul respirations (fast/deep) are compensatory CO2 off-loading to raise pH. Acetone is volatile and exhaled, producing the fruity odor.
• Hypoglycemia symptoms (tachycardia, diaphoresis, tremor) are catecholamine-driven — the body senses low glucose and releases epinephrine to trigger glycogenolysis as backup; that sympathetic surge itself produces the shakiness and sweating, preceding the neuroglycopenic symptoms (confusion, seizure) from the brain running out of fuel.
• Cerebral edema in DKA correction is a feared complication because the brain adapts to chronic hyperglycemia by accumulating intracellular osmoles; correcting blood glucose too rapidly creates an osmotic gradient that pulls free water into brain cells faster than they can adapt, particularly in pediatric DKA.
• Kussmaul respirations are a compensatory, not pathologic, finding — they represent the respiratory system's attempt to normalize pH by blowing off CO2 (respiratory compensation for a primary metabolic acidosis); suppressing this drive (e.g. with sedation) can worsen the acidemia.

Diagnostic Testing & Rule-Out Strategy

• Field: blood glucose is the single most important field test here — obtain before and after any treatment, ketone breath odor assessment, mental status trend with treatment.
• ED-level: VBG or ABG with pH (confirms and quantifies acidosis in DKA), basic metabolic panel with anion gap, serum and/or urine ketones, osmolality calculation (critical in suspected HHNS), potassium level specifically before starting insulin (insulin drives potassium intracellularly and can precipitate dangerous hypokalemia if the starting level isn't known).

Disease Reference

Scene & History

• C-spine? Fall, assisted to ground, or unknown? Head/neck/back pain?
• Loss of consciousness — how long, witnessed?
• Complaining of anything prior?
• GCS/LOC: name, location, day of week, president?
• Happened before? What was done last time, does this feel the same?
• What were they doing prior?

HAM & Delegate

• Monitor / pulse ox / vitals / oxygen / 12-lead / pupils / blood sugar / temp / lung sounds

Syncope-Specific (2nd reference)

• Witnessed? Trauma from a fall? Oral trauma?
• D-stick / 12-lead / neuro exam
• Orthostatic vitals
• Pain prior to the episode? Behavior prior to the episode?
• Knocked out or not? If so, how long?
• History — happened before? Allergies? Medications new/compliant?
• Food/fluid intake recently? Anxiety?
• AEIOU-TIPS — vasovagal is the most common cause

Screening

• Taking medications appropriately? Diabetic, on insulin?
• Last ate — when, what?
• Lightheaded or dizzy — always, or just standing?
• N/V — blood or coffee grounds? Diarrhea — blood/tarry stools?
• Headache? Blurred vision? Ringing in ears? Sensitivity to light?
• Recent trauma or falls? Recent stress or strenuous activity?
• Numbness/tingling of fingers or lips? (psychological/hyperventilation)
• Drugs or alcohol? Drinking plenty of fluids?

Females

• Chance of pregnancy? Last menstrual period, normal flow?
• Abnormal discharge — color, contents, blood? Pad count in 24 hours?
• Recent abdominal pain?

General Weakness / Flu-Like OPQRST (2nd reference)

Systems Screen for Weakness/Malaise

• Cardiac: CP, DOE, PND, edema, palpitations — 12-lead
• Pulmonary: SOB, pleuritic-type CP
• Abdominal: N/V/D, blood in vomit/stool?
• Endocrine: blood glucose, polyuria, polyphagia
• Systemic: fever/chills, weight loss, night sweats, sore throat, muscle aches
• FAST – neuro exam

Physical Exam / Check

• Orthostatics, pupils, blood sugar, CVA assessment

Serious Causes of Syncope

• MI, cardiac dysrhythmias, CVA/TIA, hypovolemic, drug use, PE, cardiac tamponade

Pathophysiology — Why We Ask

• Syncope is by definition transient with spontaneous recovery. Duration of LOC is the key discriminator: true syncope is brief (seconds — cerebral perfusion restores quickly once horizontal). Prolonged unresponsiveness points away from simple syncope toward seizure or ongoing metabolic/arrhythmic compromise.
• Orthostatic component: standing pools 500–1000mL of blood in the legs via gravity; a healthy autonomic system reflexively vasoconstricts and raises heart rate to compensate. Failure of this reflex (dehydration removing the volume to compensate with, or true autonomic dysfunction) causes orthostatic syncope.
• Cardiac preceding symptoms (palpitations, CP before passing out) flag a dysrhythmia dropping cardiac output enough to under-perfuse the brain — genuinely dangerous, since it can recur and progress toward arrest, unlike vasovagal syncope.
• The vasovagal reflex arc (most common cause) begins with a trigger (pain, emotion, prolonged standing) causing increased vagal tone and paradoxical peripheral vasodilation plus bradycardia — the opposite of the expected compensatory tachycardia, which is why the drop in cerebral perfusion is so abrupt.
• Cardiac syncope carries the highest short-term mortality of the syncope categories because the underlying arrhythmia or structural lesion causing the transient hypoperfusion can recur unpredictably and progress to sustained hemodynamic collapse or arrest.

Diagnostic Testing & Rule-Out Strategy

• Field: orthostatic vitals, 12-lead ECG (looking for conduction abnormalities, QT prolongation, WPW, Brugada pattern, or ischemia), blood glucose, thorough witness account of the event.
• ED-level: CBC (anemia/occult bleeding), troponin and BNP if cardiac cause is suspected, continuous cardiac telemetry monitoring, echocardiogram for structural heart disease (outflow obstruction, valve disease), tilt-table testing in select recurrent unexplained cases (not an acute-visit test), beta-hCG in women of childbearing age with associated abdominal symptoms.

Neuro/Movement Disorder Reference

• Multiple Sclerosis: autoimmune; numbness/paresthesias, double vision, ataxia, bladder control problems
• Muscular Dystrophies: progressive muscle weakness
• Parkinson's Disease: muscle rigidity, slowness of movement and reflexes, tremor
• Bell's Palsy: demyelination of the facial nerve; unilateral facial numbness, paralysis, decreased tearing
• Peripheral Neuropathy: sharp pain, weakness, tingling, burning, glove/sock sensation
• Spina Bifida: incomplete development of brain, spinal cord, meninges
• Chorea: irregular, unpredictable, involuntary muscle jerks impairing voluntary movement
• Dystonia: contorted posture, limbs flexed in various positions, head turned to the side

Scene & History

• C-spine? Fall or assisted to the ground? Head/neck/back pain? Unknown?
• Happened before — what was the result last time?
• Last time acting normal? Did they lose consciousness, for how long?
• What were they doing prior? Complaining of anything prior?

HAM & Delegate

• Monitor / pulse ox / vitals / oxygen + pupils / 12-lead / blood sugar / temp / lung sounds

AEIOU-TIPS

Physical Exam / Check

• Blood sugar, pupils, skin, temperature, CVA assessment, 12-lead
• D-stick / 12-lead / neuro / full primary exam / orthostatics / pain management

Most Common ALOC Causes

• Seizure, opiate overdose, hypoglycemia, CVA, trauma, hypoxia

H's & T's (Cardiac Arrest Differential Overlap)

• Hypoxia, Hypovolemia, Hydrogen Ions (acidosis), Hypo/Hyperglycemia, Hypo/Hyperthermia, Hyperkalemia
• Tablets/Toxins, Tamponade, Trauma, Tension Pneumothorax, Thrombosis (coronary/pulmonary)

Pathophysiology — Why We Ask

• AMS is a final common pathway, not a disease — consciousness requires an intact reticular activating system plus functioning cortex, both of which depend on stable substrate delivery (glucose, O2), stable chemistry (electrolytes, pH), and no structural or toxic disruption. AEIOU-TIPS systematically sweeps every category that can break one of those requirements.
• Glucose and pupils checked first because hypoglycemia and opioid toxicity (pinpoint pupils, respiratory depression) are both instantly reversible with dextrose/naloxone — fix what's fixable immediately before working the rest of the list.
• Uremia/missed dialysis: kidneys normally clear metabolic waste and maintain electrolyte/fluid balance; without dialysis, uremic toxins and fluid overload directly impair cerebral function.
• Sepsis causes global hypoperfusion and cytokine-mediated cerebral dysfunction — AMS can be a sepsis red flag even with no obvious infection source volunteered.
• Cerebral autoregulation normally keeps brain perfusion constant across a range of blood pressures; when this fails (severe hypotension, hypertensive emergency, or a structural brain lesion), consciousness becomes directly dependent on systemic hemodynamics — part of why vitals are checked before assuming a purely "medical" AMS cause.
• The reticular activating system requires both hemispheres or the brainstem itself to be dysfunctional to produce true unresponsiveness — a unilateral hemispheric lesion alone (like most strokes) usually causes focal deficits without global unresponsiveness, which is a useful discriminator between a stroke and a more diffuse process causing AMS.

Diagnostic Testing & Rule-Out Strategy

• Field: blood glucose (immediately reversible cause), pupil exam, full vitals including temperature, naloxone trial if opioid toxicity is suspected on exam.
• ED-level: comprehensive metabolic panel and ammonia level (hepatic encephalopathy), toxicology screen, CT head, blood cultures and lactate if sepsis is suspected, ABG for acid-base and CO2 status, TSH if thyroid causes are being considered in the broader differential.

Immediate Priorities

• Airway first!
• Pupils and respirations!
• Rule out trauma, seizure, dysrhythmia as contributors
• D-stick / 12-lead / neuro exam

Substance History

• What was taken? How many pills are left in the bottle?
• How much (dose), date, and route?
• Vomiting — possible aspiration?
• Other drugs or alcohol involved? OTC medications?
• When did it happen?
• Has anything already been done for the patient?

Safety Screen

• Suicidal ideation?

Pathophysiology — Why We Ask

• Toxidromes exist because different drug classes act on overlapping but distinguishable receptor systems — opioids depress the medullary respiratory centers and constrict pupils via mu-receptor activity; sympathomimetics flood adrenergic receptors causing tachycardia, hypertension, and mydriasis; anticholinergics block muscarinic receptors causing dry, flushed skin, mydriasis, tachycardia, and delirium ("mad as a hatter, red as a beet, dry as a bone").

Diagnostic Testing & Rule-Out Strategy

• Field: pupil size and reactivity, respiratory rate/depth/pattern, SpO2 and EtCO2 waveform, 12-lead ECG (QRS/QT widening from certain overdoses has direct treatment implications), blood glucose.
• ED-level: acetaminophen and salicylate levels (drawn on essentially every intentional overdose given how silently dangerous both can be early on), specific drug levels when a substance is known, ECG for QRS/QT interval measurement, basic metabolic panel and anion/osmolar gap calculation, activated charcoal candidacy assessment.

Pathophysiology — Why We Ask

• Pupils and respirations are the fastest bedside toxidrome screen: pinpoint pupils with respiratory depression suggests opioid toxicity (naloxone-reversible); dilated pupils with tachycardia/agitation suggests sympathomimetic or anticholinergic toxicity.
• Pill count and fill date let you estimate the maximum possible dose ingested — critical for anticipating toxicity timelines (e.g., delayed hepatotoxicity in acetaminophen overdose, or delayed cardiotoxicity in some cardiac medication overdoses).
• Co-ingestants (alcohol, other drugs) matter because combined CNS depressants have synergistic, not additive, respiratory depression risk.

Key Questions

• Time submerged? Water temperature? Depth of water?
• Mechanism of injury — alcohol or drugs involved?
• Head/neck/back pain?
• Gastric distention?
• Neurological deficits?

Pathophysiology — Why We Ask

• The lung injury in drowning is primarily from washout of surfactant and aspiration-induced inflammation, not from the small osmotic differences between fresh and salt water that older teaching emphasized — both mechanisms damage the alveolar-capillary membrane and can produce a delayed, ARDS-like picture hours after a seemingly stable initial presentation, which is why even asymptomatic near-drowning patients need observation.

Diagnostic Testing & Rule-Out Strategy

• Field: SpO2 and lung auscultation even in an initially well-appearing patient, core temperature, blood glucose, mental status.
• ED-level: chest X-ray, ABG for gas exchange status, observation period of several hours given the risk of delayed pulmonary deterioration, core temperature management and rewarming protocols for hypothermic patients, C-spine imaging if a diving or shallow-water mechanism raises trauma concern.

Pathophysiology — Why We Ask

• Submersion time is the primary prognostic factor — cerebral hypoxic injury accumulates with duration underwater.
• Water temperature matters because cold-water submersion can trigger the mammalian diving reflex and slows metabolic demand, occasionally allowing for meaningful neurological recovery even after longer submersion times than would otherwise be survivable.
• Gastric distention is common after submersion (swallowed water/air) and raises aspiration risk plus can impair ventilation by limiting diaphragmatic excursion.
• Mechanism/substance use screens for a primary event (diving injury — c-spine risk, or a seizure/cardiac event that caused the submersion in the first place) rather than a purely accidental drowning.

Exposure History

• Time of exposure? Exposed before?
• Hospitalized previously for a reaction? Required intubation?

Airway Screen (Highest Priority)

• Oral or facial swelling? Throat tightness? Difficulty swallowing?
• Nasal congestion? Cough?

Skin & GI

• Rashes? Hives? Itching?
• GI cramping? N/V/D?

Pathophysiology — Why We Ask

• See the allergic-reaction pathophysiology already covered above for the histamine-mediated mechanism; the key operational point is that biphasic anaphylaxis can occur, where symptoms recur hours after apparent resolution as a second wave of mediator release — the physiologic basis for extended observation after any anaphylactic episode.

Diagnostic Testing & Rule-Out Strategy

• Field: repeated airway/voice checks, SpO2, lung auscultation for developing wheeze, skin exam for progression of hives/angioedema, response to epinephrine as both treatment and diagnostic confirmation.
• ED-level: observation period (often several hours) for biphasic reaction risk, tryptase level if drawn in a reasonable post-reaction window (supports a diagnosis of anaphylaxis retrospectively), allergy/immunology referral for future identification of the trigger.

Pathophysiology — Why We Ask

• IgE-mediated mast cell degranulation releases histamine and other mediators causing vasodilation, increased capillary permeability (angioedema, hives), bronchoconstriction, and GI smooth muscle spasm (cramping, N/V/D) — the pattern of symptoms present tells you how far along the systemic reaction has progressed.
• Airway questions take priority because laryngeal/oropharyngeal edema can occlude the airway within minutes, and once swelling progresses, intubation becomes progressively more difficult — this is the finding that separates a simple allergic reaction from anaphylaxis requiring immediate epinephrine.
• Prior reaction severity/intubation history is a strong predictor — patients tend to have similar (or worsening) reaction patterns on re-exposure.

Mechanism Reference

• MVC: speed/direction/mechanism of injury/impact area/damage to vehicle/window starring
• GSW: caliber size? weapon? number of shots? range of shots? exit wounds?
• Stabbing: size of weapon? how deep did it penetrate? how many times? exit wounds?
• Falls: height of fall? hit head? head/neck/back pain? how did they land?

Delegate & Scene Approach

• C-spine / scene safety (PENMAN)
• LOC/GCS: name, location, day of week, president?
• Airway — suction? open/patent/clear/maintainable?
• Breathing — oxygen? rate/depth/ease?
• Circulation — major bleeding? pulse, skin, cap refill?
• Load and go vs. stay and play (scene time <10 min)
• Transport decision / call trauma base station
• Delegate monitor / pulse ox / vitals; cut/expose

Head-to-Toe Exam

• Head: pupils, DCAP-BLS, nasal/oral trauma
• Neck: delegate c-collar, step-offs, JVD, tracheal deviation, subcutaneous emphysema, stoma, med alert tags
• Chest: lung sounds, palpate anterior/posterior and lateral/medial, DCAP-BLS-TIC
• Abdomen: palpate for TERD, pulsating masses, soft/supple? DCAP-BLS
• Pelvic: palpate anterior/posterior, lateral to medial, incontinence/priapism, DCAP-BLS-TIC
• Legs/Arms: offset pressure, DCAP-BLS-TIC
• Feet/Hands: PMSC
• Back: palpate/check spine, thoracic/lumbar/buttocks
• Remember: c-spine/peds board, vitals, blankets, warm fluids, NG/OG

Shock Status & Fluid Reference

• Unstable: BP <90 and/or signs of inadequate tissue perfusion — start 2nd IV access
• Stable: BP >90 and/or signs of adequate tissue perfusion
• Blunt Trauma (Adult): open until stable or 2000ml max, TKO
• Penetrating Trauma (Adult): 500ml one time, TKO
• Isolated Closed Head Injury (Adult): 250ml, may repeat to max 500ml, TKO
• Morphine Pain Relief (Adult): 250ml one time, with ondansetron prophylactic
• Peds Unstable: 20ml/kg, may repeat once · Peds Stable: TKO
• Peds Morphine Pain Relief: 20ml/kg one time, with ondansetron prophylactic

Glasgow Coma Scale — Adult

• Eyes (4): Spontaneous, To Voice, To Pain, None
• Verbal (5): Oriented, Confused, Inappropriate Words, Inappropriate Sounds, None
• Motor (6): Obedient, Purposeful, Withdraws, Flexion, Extension, None

Pathophysiology — Why We Ask

• The lethal triad of trauma (hypothermia, acidosis, coagulopathy) is a self-reinforcing cycle: blood loss causes hypothermia and acidosis, both of which impair the enzymatic clotting cascade, which worsens bleeding, which worsens all three — this is the physiologic rationale behind minimizing scene time, keeping patients warm, and avoiding excessive crystalloid dilution of clotting factors.
• Compensated vs. decompensated shock in trauma reflects how much blood volume has been lost before vital signs change — young, healthy patients can lose up to 30% of blood volume while maintaining a near-normal blood pressure through peripheral vasoconstriction and tachycardia, meaning a "normal" BP does not rule out significant ongoing hemorrhage.

Diagnostic Testing & Rule-Out Strategy

• Field: primary survey (ABCDE), GCS, focused neurovascular checks distal to any deformity, serial vital sign trends rather than a single reading.
• ED-level: FAST exam (rapid bedside ultrasound for free fluid in the abdomen, pelvis, and pericardium), CT imaging per mechanism (head, C-spine, chest, abdomen/pelvis), CBC and type & screen/crossmatch, coagulation studies, lactate as a marker of tissue hypoperfusion, serial hemoglobin/hematocrit to trend occult blood loss.

Glasgow Coma Scale — Infant

• Eyes (4): Spontaneous, To Speech, To Pain, None
• Verbal (5): Coos/Babbles, Irritable Cry, Cries to Pain, Moans to Pain, None
• Motor (6): Moves Purposefully/Spontaneously, Withdraws to Touch, Withdraws to Pain, Flexion, Extension, None

Rule Out (Medical Cause of the Fall)

• Dysrhythmia, seizure, blood glucose, anti-hypertensive medications, narcotics, diuretics

History & Exam

• OPQST / DCAP-BTLS
• Witnessed? Knocked out or not?
• Complaints prior to the fall — weakness, dizziness, difficulty breathing, vomiting, diarrhea? (vasovagal)
• What were they doing? How did it happen?
• Surface fallen upon? Distance of the fall?
• Assisted fall? Recent fall history?

Pathophysiology — Why We Ask

• Falls in older adults disproportionately cause serious injury because age-related changes — bone density loss (osteoporosis), reduced subcutaneous tissue cushioning, and blunted baroreceptor reflexes — combine to make both the fall itself more likely and the resulting injury more severe for the same mechanical energy as in a younger patient.

Diagnostic Testing & Rule-Out Strategy

• Field: blood glucose and orthostatic vitals to screen for a medical cause of the fall, 12-lead ECG, focused exam of the injured area plus a search for injury the patient may not have noticed given distraction from a more obvious complaint.
• ED-level: imaging targeted to the mechanism and exam (hip/pelvis X-ray in older adults is a common miss if not specifically screened for), CT head if on anticoagulants or if any LOC/anticoagulant use is present given the low threshold for occult intracranial bleeding in this population, ECG and troponin if a cardiac cause of the fall is suspected.

Pathophysiology — Why We Ask

• Falls in adults — especially older adults — are frequently a symptom of an underlying medical event (arrhythmia, hypoglycemia, orthostatic medication effect) rather than a purely mechanical trip. Treating every fall as "just a fall" risks missing the syncope, dysrhythmia, or stroke that caused it.
• Distance and surface determine the energy transferred and thus injury pattern probability — a fall from standing height onto carpet is a very different risk profile than a fall from a ladder onto concrete.

Head Injury

• Mechanism of injury
• Neuro exam; head/neck/back pain?
• Obvious open wound? DCAP-BTLS to the scalp? Fractures to the skull?
• Raccoon eyes? Battle's sign? CSF leak?
• Neurological deficits?
• Knocked out — how long? Fall — how far, onto what?
• Amnesia? Seizure activity?
• Irregular respirations? Weak/dizzy? Blood glucose?
• Visual complaints? Posturing? N/V?

Spinal Injury

• DCAP-BTLS / OPQRST / full neuro exam
• Pain along the spine? Step-offs?
• Sensory/motor deficits? Deformity of the spine?
• LOC — how long? Fall — how far, landed on what?
• Priapism? Posturing? Loss of bowel control?
• Hypotension? Normal heart rate? Flushed extremities?

Pathophysiology — Why We Ask

• Raccoon eyes/Battle's sign/CSF leak are signs of a basilar skull fracture — periorbital and mastoid ecchymosis result from blood tracking along fascial planes from a fracture at the skull base, and CSF leakage (otorrhea/rhinorrhea) means the dura has been breached.
• Posturing (decorticate/decerebrate) reflects the level of brainstem dysfunction from rising intracranial pressure — decerebrate (extension) generally indicates a more caudal/severe injury than decorticate (flexion).
• Irregular respirations can reflect brainstem compression from herniation — a late and ominous sign of rising ICP.
• Priapism, flushed extremities, and hypotension with a normal (not elevated) heart rate are classic signs of neurogenic shock — spinal cord injury disrupting sympathetic outflow causes vasodilation below the injury level without the expected compensatory tachycardia.
• Bowel/bladder loss and sensory/motor deficits localize the level and completeness of a spinal cord injury.

Diagnostic Testing & Rule-Out Strategy

• Field: serial GCS (a single number matters less than the trend), pupil exam, motor/sensory exam of all four extremities, vital sign pattern (Cushing's triad — hypertension, bradycardia, irregular respirations — is a late sign of rising ICP/herniation).
• ED-level: non-contrast CT head (first-line for structural injury/bleed), CT C-spine per clinical decision rules (NEXUS or Canadian C-Spine), MRI if ligamentous or cord injury is suspected with a normal CT, coagulation studies particularly if on anticoagulants given elevated intracranial bleeding risk.

Key Questions

• Mechanism of injury
• OPQRST
• 12-lead — rule out a cardiac relation to the injury
• Obvious open wound? Pain at the site of injury?
• Pleuritic chest pain?
• Bruising to the chest wall? Crepitus on palpation?
• Penetration injury?
• Dyspnea? Hemoptysis?
• Unequal chest rise/fall?

Pathophysiology — Why We Ask

• Tension pneumothorax physiology: a one-way valve effect lets air enter the pleural space on inspiration but not escape on expiration, progressively raising intrapleural pressure until it collapses the ipsilateral lung, shifts the mediastinum, kinks the great vessels, and drops venous return — obstructive shock develops from mechanical vena cava compression, not blood loss.
• Flail chest causes paradoxical chest wall movement because the free-floating segment is no longer mechanically linked to the rest of the thoracic cage — it moves inward on inspiration (when the rest of the chest expands) and outward on expiration, reducing effective tidal volume independent of any underlying lung contusion, which is often the bigger driver of hypoxia in these patients.

Diagnostic Testing & Rule-Out Strategy

• Field: repeated lung auscultation bilaterally, palpation for crepitus/subcutaneous emphysema, tracheal position, SpO2 trend, needle decompression is a field diagnostic-and-treatment maneuver for suspected tension pneumothorax based on clinical findings alone — it is not an imaging-confirmed diagnosis in the field.
• ED-level: chest X-ray, bedside ultrasound (absent lung sliding for pneumothorax, pericardial fluid for tamponade), CT chest for occult injury not visible on plain film, ECG and troponin if blunt cardiac injury is suspected from the mechanism.

Pathophysiology — Why We Ask

• Crepitus on palpation indicates subcutaneous emphysema — air has escaped from an injured lung/airway into the tissue planes, and is a marker for underlying pneumothorax or tracheobronchial injury.
• Unequal chest rise/fall can indicate flail chest (a segment of ribs fractured in multiple places moving paradoxically) or a large pneumothorax collapsing one side.
• Open wound with penetrating mechanism raises concern for an open ("sucking") pneumothorax and for direct cardiac/great vessel injury depending on the wound's location relative to the "box" (nipples, clavicles, epigastrium).
• Hemoptysis suggests pulmonary parenchymal or airway injury with bleeding into the alveolar/bronchial space.

Key Questions

• Mechanism of injury; pain? OPQRST
• Obvious open wound? Pain at the site of injury?
• Bruising over the abdomen?
• Firmness upon palpation? Tenderness on palpation?
• Distention? Rigidity?
• Evisceration?
• Signs of shock?

Pathophysiology — Why We Ask

• The abdomen can conceal a large volume of blood loss because the peritoneal cavity has substantial compliance — several liters can accumulate before physical distention becomes obvious, which is exactly why unexplained shock after abdominal trauma is treated as intra-abdominal hemorrhage until proven otherwise.

Diagnostic Testing & Rule-Out Strategy

• Field: serial abdominal exams (findings can evolve over the transport time), vital sign trend as the primary clue to occult hemorrhage, mechanism-based index of suspicion even with a benign initial exam.
• ED-level: FAST exam for free fluid, CT abdomen/pelvis with IV contrast in a stable patient, immediate operative exploration in an unstable patient with a positive FAST rather than awaiting CT, serial hemoglobin/hematocrit trends, type & crossmatch.

Pathophysiology — Why We Ask

• Firmness/rigidity/distention together suggest ongoing intra-abdominal hemorrhage or peritoneal irritation — blood or bowel contents in the peritoneal cavity irritates the parietal peritoneum, producing involuntary guarding (rigidity) that the patient can't relax even when asked.
• Evisceration (organs protruding through the wound) is managed by covering with a moist sterile dressing — never attempting to replace the organs, which risks further contamination and vascular compromise.
• Signs of shock without obvious external bleeding should raise strong suspicion for occult intra-abdominal hemorrhage — the abdomen can hold a large volume of blood loss before external signs (distention) become obvious.

Key Questions

• Mechanism of injury; OPQRST; DCAP-BTLS
• Open or closed? Exposed bone fragment?
• Deformities? Tenderness on palpation?
• Swelling? Bruising? Crepitus?
• Pain on movement? Loss of movement?
• Numbness? Paresthesia?
• Pallor? Pulses?

Pathophysiology — Why We Ask

• Compartment syndrome develops because fascia surrounding a muscle compartment is relatively non-elastic — bleeding or swelling within that fixed space raises pressure until it exceeds capillary perfusion pressure, cutting off blood flow to nerve and muscle even though a distal pulse may still be palpable early on (pulselessness is a very late finding, not an early one).

Diagnostic Testing & Rule-Out Strategy

• Field: pulse, motor, and sensory (PMS) checks before and after any splinting, comparison to the uninjured side, reassessment after any patient movement.
• ED-level: plain X-ray of the injured area, compartment pressure measurement if compartment syndrome is clinically suspected (a clinical diagnosis primarily, with pressure measurement supporting it), CT or MRI for complex fractures or suspected ligamentous/soft tissue injury not well seen on plain film, vascular studies (CT angiogram or Doppler) if a pulse deficit or hard signs of vascular injury are present.

Pathophysiology — Why We Ask

• Pallor, pulselessness, paresthesia distal to an injury are signs of vascular compromise — a fracture or dislocation can directly injure or compress an adjacent artery, and prolonged ischemia risks limb loss, making this a time-critical reassessment finding before and after any splinting.
• Open vs. closed matters because an open fracture (bone breaking skin, or skin breaking over the fracture site) carries significant infection risk and generally requires more urgent surgical management.
• Crepitus is the palpable/audible grinding of fractured bone ends and is a reliable sign of fracture even without visible deformity.

Vehicle & Scene Assessment

• Damage to the vehicle (passenger space intrusion / PSI)?
• Steering wheel damage?
• Airbag deployed? Was the patient ambulatory?
• Speed? Seatbelt use?
• Spidering/starring on the windshield?

Patient Assessment

• Vomiting?
• Knocked out — before or after the collision?
• Do they remember the event?
• Head/neck/back pain?
• OPQRST / DCAP-BTLS / HAM
• Neuro exam, c-spine or CSM (circulation/sensation/motor) assessment
• Drugs/alcohol involved?

Pathophysiology — Why We Ask

• Second-collision physiology: in a crash, the vehicle stops first (first collision), the occupant's body continues moving until restrained or struck by an interior surface (second collision), and internal organs continue moving within the body until restrained by their ligamentous attachments (third collision) — this is why internal organ injury (aortic tear, solid organ laceration) can occur without any external chest wall injury.

Diagnostic Testing & Rule-Out Strategy

• Field: mechanism documentation (vehicle damage, restraint use, intrusion) communicated to the receiving facility since it directly informs their imaging threshold, full primary and secondary survey, serial vitals.
• ED-level: CT imaging guided by mechanism severity even with a reassuring initial exam given high-energy mechanisms' potential for occult injury, FAST exam, chest X-ray screening for a widened mediastinum (aortic injury), pelvic X-ray or CT for pelvic ring injury.

Pathophysiology — Why We Ask

• Steering wheel deformity and windshield starring are physical evidence of where the occupant's body absorbed kinetic energy — they predict chest/cardiac contusion (steering wheel) or head/facial/c-spine injury (windshield) even before the exam finds anything.
• KO before vs. after the collision helps distinguish a medical event that caused the crash (e.g., syncope, seizure, MI) from a purely traumatic loss of consciousness from impact.
• Passenger space intrusion is one of the strongest predictors of high-energy transfer and significant occult injury, even in a patient who looks stable on scene.

Priority

• Determine TBSA and make the transport decision
• ABCs — airway is the priority in facial burns/suspected inhalation injury

Pediatric Fluid Resuscitation

• Unstable: 20ml/kg, may repeat once
• Stable: ≤5 = 150ml/hr · >5 but <15 = 250ml/hr

Pediatric Destination Criteria

• Closest – Minor: <5% TBSA, <2% full thickness
• Closest – Moderate: 5–10% TBSA, 2–5% full thickness; high-voltage injury, suspected inhalation injury, circumferential burn, predisposing medical problems
• Burn Center – Major: >10% TBSA, >5% full thickness; high-voltage burn, known inhalation, significant burn to face/eyes/ears/genitalia/joints

Adult Fluid Resuscitation

• Unstable: 250ml up to 1000ml
• Stable: 500ml/hr

Adult Destination Criteria

• Closest – Minor: <10% TBSA, <2% full thickness
• Closest – Moderate: 10–20% TBSA, 2–5% full thickness; high-voltage injury, suspected inhalation burn, circumferential burn, predisposing medical problems
• Burn Center – Major: >20% TBSA, >5% full thickness; high-voltage burn, known inhalation injury, significant burn to face/eyes/ears/genitalia/joints

Pathophysiology — Why We Ask

• TBSA and depth predict fluid loss through the burned skin barrier and systemic inflammatory response — larger/deeper burns lose proportionally more plasma volume, driving hypovolemic shock if under-resuscitated.
• Circumferential burns risk compartment-syndrome-like compression as underlying tissue swells against non-elastic eschar — a limb or the chest wall can lose perfusion or ventilatory capacity even without any airway or vascular injury elsewhere.
• Inhalation injury risk is why airway is prioritized: heat and toxic combustion products injure the airway mucosa, and swelling can progress over hours to complete obstruction — early definitive airway management matters even before visible distress develops.

Diagnostic Testing & Rule-Out Strategy

• Field: TBSA estimation (rule of nines or palm method), airway assessment for singed nasal hairs/soot/hoarseness suggesting inhalation injury, SpO2 (note: pulse oximetry can be falsely reassuring in carbon monoxide poisoning since standard SpO2 cannot distinguish oxyhemoglobin from carboxyhemoglobin).
• ED-level: carboxyhemoglobin level (specifically requested, not reflected in standard SpO2) and cyanide level if enclosed-space fire exposure, ABG, chest X-ray, bronchoscopy if inhalation injury is strongly suspected, fluid resuscitation calculations formalized using validated formulas (e.g. Parkland) based on measured TBSA and weight.