STAT Stitch Deep Dive Podcast Beyond The Bedside

STAT Stitch Deep Dive Podcast Beyond The Bedside

di Regular Guy

Corsi Scienza della vita

Stagione 7

VS CC | DKA V HHS

1. DM Classification & Core Diagnostics Type 1 DM: Autoimmune β-cell destruction (HLA-DR3/DR4) causing absolute insulin deficiency; presents abruptly with classic 3 Ps (polyuria, polydipsia, polyphagia), weight loss, and DKA risk[1][2]. Type 2 DM: Insulin resistance combined with relative β-cell deficiency and inappropriate hepatic glucose production[3]. Onset is gradual[4]. Diagnostic Criteria: A1C ≥6.5%, Fasting Plasma Glucose ≥126 mg/dL, 2-hr OGTT ≥200 mg/dL, or Random Glucose ≥200 mg/dL with classic symptoms[5]. Glycemic target A1C is <7.0%[6]. 2. High-Yield Pharmacotherapy & Insulin Dynamics Insulin Types: Rapid-acting (lispro, aspart; onset 10–30 min, mealtime bolus), Short-acting (Regular; onset 30–60 min, only IV insulin), Intermediate (NPH; peaks 4–12 hr, cloudy), Long-acting (glargine, detemir; peakless basal)[7]. Basal-Bolus Strategy: Optimal plan mimicking normal endogenous insulin secretion[7]. Key Oral Agents: Metformin (Biguanide) reduces hepatic glucose output[10]. Safety Alert: Discontinue metformin 48 hr before/after IV contrast to prevent acute kidney injury and lactic acidosis[10][11]. Sulfonylureas (glipizide) stimulate insulin release and carry high hypoglycemia risk[11][12]. 3. Hyperglycemic Emergencies: DKA vs. HHS DKA (T1DM): Absolute insulin deficiency → uncontrolled lipolysis → ketone bodies → metabolic acidosis (pH <7.30, HCO₃⁻ <16 mEq/L), Kussmaul respirations, fruity breath, glucose >250 mg/dL[13][14]. HHS (T2DM): Enough circulating insulin prevents ketosis, but severe hyperglycemia (>600 mg/dL) causes osmotic diuresis, hyperosmolality, and profound neurologic deficits (coma, seizures)[15][16]. Emergency Treatment Protocol:IV Fluids: First priority. 0.9% NaCl (1 L/hr) to maintain urine output (30–60 mL/hr)[14][15]. Add 5%–10% dextrose when glucose reaches ~250 mg/dL to prevent hypoglycemia and cerebral edema[14][15]. Potassium: Check K⁺ BEFORE starting insulin. Insulin shifts K⁺ intracellularly, causing life-threatening hypokalemia if uncorrected[15]. Continuous IV Regular Insulin: 0.1 U/kg/hr; target glucose reduction of 36–54 mg/dL/hr[15]. 4. Hypoglycemia & Chronic Complications Hypoglycemia (<70 mg/dL): Treat via Rule of 15 (15–20g fast-acting carbs, recheck in 15 min)[16][17]. Unconscious: 20–50 mL 50% Dextrose IV or 1 mg Glucagon IM/SQ (turn on side to prevent aspiration)[17]. Chronic Complications: Driven by angiopathy[18]. Macrovascular (CVD, stroke, PAD) managed via BP (<140/90) and lipid control[19]. Microvascular annual screening: Retinopathy (dilated eye exam), Nephropathy (urine albumin/creatinine; treat with ACEi/ARBs), and Neuropathy (monofilament test, daily foot inspection)[20].

CC CJM | GU

Urinary System: 80/20 Summary 1. Anatomy & Blood Supply The upper urinary tract has two retroperitoneal, bean-shaped kidneys (T12–L3) and 2 ureters[1]. The lower tract comprises the bladder and urethra[1]. Each kidney is shielded by a fibrous capsule and cushioned by fat[1]. The functional unit is the nephron (~1 million), consisting of a glomerulus, Bowman's capsule, and tubule system (PCT, loop of Henle, DCT, and collecting ducts)[2]. Blood flow is ~1200 mL/min (20-25% of cardiac output) via the renal artery, which divides into afferent arterioles[2]. 2. Physiology of Urine Formation Urine is formed through filtration, reabsorption, secretion, and excretion[2]. Glomerular Filtration: Hydrostatic pressure filters blood across a porous, semipermeable membrane into Bowman’s capsule, yielding a filtrate lacking cells and large proteins[3]. Normal Glomerular Filtration Rate (GFR) is ~125 mL/min; only ~1 mL/min is excreted as urine[3]. Tubular Function:PCT: Reabsorbs 80% of electrolytes and water, all glucose, amino acids, and bicarbonate; secretes H+ and creatinine[4]. Loop of Henle: Conserves water and concentrates filtrate. Descending loop is water-permeable; ascending limb actively reabsorbs Cl- and Na+ (25% of sodium load) and is water-impermeable[4]. DCT & Collecting Ducts: Finalize regulation of water (controlled by ADH, which increases permeability) and acid-base balance (reabsorbing HCO3- and secreting H+)[4][5]. Aldosterone promotes Na+ and water reabsorption in exchange for K+ excretion[5]. Atrial Natriuretic Peptide (ANP) opposes this by increasing Na+ excretion and GFR[5]. 3. Hormonal & Regulatory Functions Erythropoietin: Released during hypoxia or hypoperfusion, stimulating RBC production (deficient in renal failure, causing anemia)[5]. RAAS: Juxtaglomerular cells release renin during hypoperfusion, low BP, or hyponatremia. Renin converts angiotensinogen to angiotensin I, which ACE converts to angiotensin II—causing vasoconstriction and aldosterone release[6]. Prostaglandins (PGE2, PGI2): Medullary vasodilators that maintain renal blood flow and counteract vasoconstrictors[7]. Vitamin D: Kidneys perform the final activation step of vitamin D, essential for calcium absorption[5]. 4. Diagnostics & Assessment Key Labs: Serum creatinine is the most reliable renal function index (released at a constant rate from muscle)[8][9]. Creatinine clearance (24-hr urine) approximates GFR[9][10]. BUN rises with dysfunction but is altered by protein intake, tissue breakdown, and hydration[8]. Physical Exam: Involves palpation of the right kidney and indirect fist percussion of the costovertebral angle (CVA) to elicit pain in infection or obstruction[11][12]. Nephrotoxic Risks: Drugs like aminoglycosides, NSAIDs, and contrast media are highly nephrotoxic[13]. Dehydration increases the risk of contrast-induced nephropathy[9].

CC CJM | DKA v HHS

. DM Classification & Core Diagnostics Type 1 DM: Autoimmune β-cell destruction (HLA-DR3/DR4) causing absolute insulin deficiency; presents abruptly with classic 3 Ps (polyuria, polydipsia, polyphagia), weight loss, and DKA risk[1][2]. Type 2 DM: Insulin resistance combined with relative β-cell deficiency and inappropriate hepatic glucose production[3]. Onset is gradual[4]. Diagnostic Criteria: A1C ≥6.5%, Fasting Plasma Glucose ≥126 mg/dL, 2-hr OGTT ≥200 mg/dL, or Random Glucose ≥200 mg/dL with classic symptoms[5]. Glycemic target A1C is <7.0%[6]. 2. High-Yield Pharmacotherapy & Insulin Dynamics Insulin Types: Rapid-acting (lispro, aspart; onset 10–30 min, mealtime bolus), Short-acting (Regular; onset 30–60 min, only IV insulin), Intermediate (NPH; peaks 4–12 hr, cloudy), Long-acting (glargine, detemir; peakless basal)[7]. Basal-Bolus Strategy: Optimal plan mimicking normal endogenous insulin secretion[7]. Key Oral Agents: Metformin (Biguanide) reduces hepatic glucose output[10]. Safety Alert: Discontinue metformin 48 hr before/after IV contrast to prevent acute kidney injury and lactic acidosis[10][11]. Sulfonylureas (glipizide) stimulate insulin release and carry high hypoglycemia risk[11][12]. 3. Hyperglycemic Emergencies: DKA vs. HHS DKA (T1DM): Absolute insulin deficiency → uncontrolled lipolysis → ketone bodies → metabolic acidosis (pH <7.30, HCO₃⁻ <16 mEq/L), Kussmaul respirations, fruity breath, glucose >250 mg/dL[13][14]. HHS (T2DM): Enough circulating insulin prevents ketosis, but severe hyperglycemia (>600 mg/dL) causes osmotic diuresis, hyperosmolality, and profound neurologic deficits (coma, seizures)[15][16]. Emergency Treatment Protocol:IV Fluids: First priority. 0.9% NaCl (1 L/hr) to maintain urine output (30–60 mL/hr)[14][15]. Add 5%–10% dextrose when glucose reaches ~250 mg/dL to prevent hypoglycemia and cerebral edema[14][15]. Potassium: Check K⁺ BEFORE starting insulin. Insulin shifts K⁺ intracellularly, causing life-threatening hypokalemia if uncorrected[15]. Continuous IV Regular Insulin: 0.1 U/kg/hr; target glucose reduction of 36–54 mg/dL/hr[15]. 4. Hypoglycemia & Chronic Complications Hypoglycemia (<70 mg/dL): Treat via Rule of 15 (15–20g fast-acting carbs, recheck in 15 min)[16][17]. Unconscious: 20–50 mL 50% Dextrose IV or 1 mg Glucagon IM/SQ (turn on side to prevent aspiration)[17]. Chronic Complications: Driven by angiopathy[18]. Macrovascular (CVD, stroke, PAD) managed via BP (<140/90) and lipid control[19]. Microvascular annual screening: Retinopathy (dilated eye exam), Nephropathy (urine albumin/creatinine; treat with ACEi/ARBs), and Neuropathy (monofilament test, daily foot inspection)[20].

CC CJM | Blood Disorders

Clinician’s 80/20 Hematologic & Anemia Summary Core Clinical Concepts Blood disorders disrupt homeostasis. Key pathological threads include: Fatigue: Secondary to tissue hypoxia (anemia, cancer). Infection Risk: Compromised immunity and risk for infection is a major concern in hematologic cancers and a common side effect of therapy. Pain: Common and classic in sickle cell disease (SCD) and oncology. Perfusion & Clotting: Excessive clotting impairs perfusion; inadequate clotting causes blood loss and fluid volume deficit[1]. Anemia: Definition & Pathophysiology Anemia is not a disease but a manifestation of an underlying pathologic process[2]. It is defined as a deficit in red blood cell (RBC) count, hemoglobin (Hgb) quantity/quality, and/or volume of packed red blood cells (hematocrit)[2]. Tissue hypoxia drives all clinical findings[3]. The body compensates via cardiopulmonary escalation, increasing heart rate (HR) and stroke volume to maintain cardiac output (CO)[4]. Low blood viscosity contributes to systolic murmurs and bruits[4]. If O2 demand exceeds supply, angina or MI occurs[4]. Chronic overwork leads to heart failure (HF), cardiomegaly, congestion, and peripheral edema[4]. Diagnostics & Classification Diagnostics rely on CBC, reticulocyte count, and peripheral smear[2]. Anemia is classified by: Morphology (RBC size/color): Most accurate framework[5]. Normocytic, Normochromic (MCV 80–95 fL, MCH 27–31 pg): Caused by acute blood loss, hemolysis, CKD, cancers, or SCD[6]. Microcytic, Hypochromic (MCV <80 fL, MCH <27 pg): Caused by iron deficiency, thalassemia, lead poisoning, B6/copper deficiency[6]. Macrocytic, Normochromic (MCV >95 fL, MCH >31 pg): Caused by B12 (cobalamin) deficiency, folic acid deficiency, or liver disease[6]. Etiology (Cause): Best for structuring care[5]. Divided into decreased RBC production, blood loss, or increased RBC destruction (hereditary like SCD/G6PD vs. acquired like DIC, HELLP, prosthetic valves, or bypass)[7]. Severity & Clinical Manifestations Symptoms depend on onset speed, severity, and Hgb level[3]: Mild (Hgb 10–12 g/dL): Often asymptomatic. Heavy exercise triggers compensatory palpitations, mild fatigue, and dyspnea[3]. Moderate (Hgb 6–10 g/dL): Cardiopulmonary symptoms (dyspnea, palpitations) occur both during activity and at rest[11]. Severe (Hgb <6 g/dL): Multi-system decompensation occurs[11].Integumentary: Pallor (shunted blood flow), jaundice (bilirubin from RBC hemolysis), and severe itching (accumulation of skin bile)[11]. Cardiopulmonary: Marked tachycardia, angina, murmurs, and congestive failure[4].

CC CJM | Neuro Assessment

80/20 Neurological Assessment & Physiology Summary 1. Structure & Cellular Biology Organization: The CNS consists of the brain, spinal cord, and CN I-II[1]. The PNS contains CN III-XII, spinal nerves, and the ANS[1]. Cells & Myelin: Neurons conduct action potentials via saltatory conduction across nodes of Ranvier, accelerated by myelin[2]. Astrocytes form the blood-brain barrier and create scar tissue (gliosis) upon injury[2]. Oligodendrocytes myelinate CNS axons; Schwann cells myelinate PNS axons[2][3]. Synapses: Neurotransmitters cross synapses to alter impulse transmission, using excitatory (glutamate) or inhibitory (GABA) pathways[4]. 2. Pathways, Lobes & Perfusion Tracts: Ascending tracts carry sensory input (spinothalamic for pain/temp; dorsal columns for touch, vibration, position)[5]. Descending tracts (corticospinal) carry motor output[5]. Motor Lesions: UMN lesions cause spasticity, hyperreflexia, and weakness[6]. LMN lesions cause flaccidity, hyporeflexia, and muscle atrophy[6]. Cerebral Lobes: Frontal lobe controls cognition and motor speech (Broca's)[7]. Parietal lobe senses sensory data[7]. Temporal lobe handles hearing/language (Wernicke's); occipital processes vision[7]. Perfusion: Anterior circulation stems from carotids; posterior from vertebral-basilar systems, joining at the circle of Willis[8]. 3. Bedside Assessment Mental Status: Ongoing check of consciousness, orientation, cognition, and mood/affect[9]. Cranial Nerves: CN III, IV, VI coordinate eye movements[10]. Pupil non-constriction (CN III) is an early sign of brain herniation[10]. Corneal reflex tests CN V/VII[11]. Gag reflex tests CN IX/X; a weak gag risks aspiration[12]. Midline tongue protrusion checks CN XII[12]. Sensory & Proprioception: Test touch, pain, vibration, and digit position[13][14]. A positive Romberg test indicates posterior column dysfunction[15]. Reflexes: Deep tendon reflexes are graded 0–5[15]. An extensor plantar response (toes up) signals an abnormal UMN lesion[16]. 4. Diagnostics & Nursing Interventions CSF Analysis: Normal CSF is clear/colorless, with pressure of 60–150 mm H2O, protein of 15–45 mg/dL, and glucose of 40–70 mg/dL[16]. Lumbar Puncture (LP) Care: LP is contraindicated in increased ICP due to risk of herniation[17]. Pre-procedure, check coagulation and place the patient in a sitting/side-lying flexed position[18][19]. Post-procedure, keep flat, monitor for headache, and push fluids[18]. Aging: Aging causes cerebral atrophy, wider ventricles, reduced blood flow, and demyelination[20]. This leads to orthostatic hypotension, poor thermoregulation, and high fall risks[20][21].

CC CJM | CKD v AKI

80/20 Clinical Summary: Renal Failure (AKI vs. CKD) 1. Pathophysiology AKI: Sudden, potentially reversible decline in GFR[1].Prerenal: Decreased perfusion (hypovolemia, shock, HF). Oliguria occurs without tissue damage; reversible with fluids[1][2]. Intrarenal: Direct tissue damage, 90% from Acute Tubular Necrosis (ATN) (ischemia, sepsis, nephrotoxins)[2]. Postrenal: Mechanical obstruction (BPH, calculi) causing urine reflux[3]. CKD: Gradual, irreversible nephron loss (GFR <60 for >3 months)[4]. Primary causes: Diabetes (50%), Hypertension (25%)[4]. Stage 5 (ESRD) GFR <15[5]. 2. Clinical Phases & Manifestations AKI Phases:Oliguric (<400 mL/d): Fluid overload (edema, hypertension, pulmonary edema), acidosis, hyperkalemia (ECG: peaked T, wide QRS), and uremia[3][6]. Diuretic (1–5+ L/d): Osmotic diuresis (high urea). Risk of hypovolemia, hypotension, hyponatremia, and hypokalemia[7]. Recovery: GFR increases, BUN/Creatinine stabilize (takes up to 12 months)[7]. CKD Manifestations (Uremia):Cardiovascular: Leading cause of death; due to vascular calcification, volume overload, and hypertension[8][9]. Hematologic: Anemia from decreased erythropoietin[10]. CKD-MBD: Low active Vitamin D reduces calcium absorption[11]. Hypocalcemia triggers PTH release, causing bone demineralization (osteomalacia, osteitis fibrosa) and calcifications[12]. 3. Diagnostics & Priority Interventions Metrics: GFR is the best indicator of kidney function[8][13]. Creatinine is the best AKI marker[6]. Proteinuria is first sign of CKD[13]. Hyperkalemia Emergency Care:Cardioprotection: IV Calcium Gluconate (stabilizes myocardium)[14]. Shift K+ Intracellularly: IV Regular Insulin + Glucose, or IV Sodium Bicarbonate[14]. Definitive Removal: Hemodialysis or Kayexalate (avoid in paralytic ileus due to bowel necrosis)[14][15]. Fluid Limits: Oliguric AKI: previous 24-hr loss + 600 mL[14]. Anemia: Exogenous EPO. Monitor for hypertension, clots; supplement iron[16]. 4. RRT & Post-Op Care HD: Rapid fluid/solute shifts. Assess AV Fistula for thrill and bruit[17]. Safety: No BP/blood draws/IVs in access arm[18]. Complication: Hypotension, cramps[19]. PD: Uses peritoneal membrane. Core complication: Peritonitis (abdominal pain, rebound tenderness, cloudy effluent)[20][21]. CRRT: Slow, continuous solute/fluid removal for hemodynamically unstable AKI[22][23]. Transplantation: Post-op priority is fluid/electrolyte balance[24]. Watch for massive diuresis (replace mL-for-mL) or ATN[24]. CVD is the leading cause of death post-transplant[25].

CC CJM | Stroke [CVA]

80/20 Clinical Stroke Summary Core Concepts & Emergency Recognition A stroke is an emergency where cell death occurs due to ischemia (inadequate blood flow, 87% of cases) or hemorrhage (bleeding, 13%)[1][2]. Interruption of blood flow alters brain metabolism in 30 seconds, stops it in 2 minutes, and causes cell death in 5 minutes[3]. The FAST protocol is critical for rapid recognition: Face drooping, Arm weakness/drift, Speech difficulties, and Time of symptom onset (critical for determining treatment eligibility)[1]. Pathophysiology & Classification Ischemic Stroke: Divided into Thrombotic (60% of cases; associated with hypertension, diabetes, and atherosclerosis; symptoms develop slowly/stepwise)[2][6] and Embolic (clot from the heart, often due to atrial fibrillation, travels and occludes a cerebral artery; onset is sudden with severe deficits)[2]. Hemorrhagic Stroke: Includes Intracerebral (bleeding into brain tissue, mostly caused by hypertension)[2]and Subarachnoid (SAH) (bleeding into CSF-filled space, often from ruptured aneurysms)[9]. SAH can trigger severe vasospasms, peaking 6–10 days post-bleed[10]. Key Diagnostics & Triage Immediate noncontrast head CT or MRI is mandatory to rapidly differentiate ischemic from hemorrhage[4]. The NIH Stroke Scale (NIHSS) (scores 0–42) is the primary clinical tool to document baseline severity and track neurologic changes[11][12]. Acute Interventions & Hemodynamic Targets Ischemic: IV tPA must be given within 3 to 4.5 hours of symptom onset after screening out hemorrhage, active bleeding, or recent trauma[13]. Endovascular therapy with stent retrievers is highly effective[14]. Keep BP <185/110 mmHg before tPA, and <180/105 mmHg for 24 hours after[5]. If ineligible for tPA, lower BP only if SBP >220 or DBP >120 mmHg[5]. Hemorrhagic: Anticoagulants and antiplatelets are strictly contraindicated[14]. Manage hypertension to maintain SBP <160 mmHg[14]. For SAH, administer the calcium channel blocker nimodipine to prevent vasospasm[11][15]. High-Priority Nursing ADPIE Actions Airway & Aspiration: Keep the patient NPO until a formal swallowing screen is completed within 24 hours to prevent aspiration pneumonia[5]. ICP Management: Elevate the head of bed 30°, keep head/neck in midline, and avoid hip flexion to maximize venous drainage and reduce intracranial pressure[13][16]. Safety & Pattern Recognition: Left-brain stroke causes right hemiplegia, aphasia, slow/cautious behavior, and depression[18]. Right-brain stroke causes left hemiplegia, spatial-perceptual neglect, and highly impulsive, safety-compromising behavior[18][19]. Protect from injury and address one-sided neglect[19][20]. VTE Prophylaxis: Implement passive/active range of motion, sequential compression devices, and low-molecular-weight heparin[21].

CC CJM | Chronic Neurological Disorders

Primary Headaches[1] Tension (TTH): Bilateral, dull bandlike pressure[1][2]. No nausea[2]. Tx: NSAIDs[3][4]. Prev: Amitriptyline[3][5]. Migraine: Unilateral throbbing, ± aura[1][6]. Triggers: stress, red wine[6][7]. Acute: Triptans (sumatriptan; contraindicated in CAD, ischemic stroke, uncontrolled HTN)[5]. Prev: Topiramate, β-blockers, Botox[3]. Cluster: Severe unilateral orbital pain in clusters[1][4]. ptosis, tearing[1][4]. Tx: High-flow 100% O2 (7-12 L/min)[3][8], triptans[8]. Prev: Verapamil[8]. Medication Overuse (MOH): Daily headache from analgesic overuse. Tx: Stop drug[8]. Seizure Disorders[9] Def: ≥2 unprovoked seizures >24h apart[9]. Classes: Generalized (bilateral hemispheres, e.g., tonic-clonic with LOC[10][11]) vs. Focal (1 hemisphere, aware vs. impaired[10][12]). Status Epilepticus (SE): Seizure >5 min or recurrent; emergency[12]. Tx: IV Lorazepam, then fosphenytoin[13]. Nursing Care: Airway, turn on side, do not restrain, never insert objects in mouth, pad rails, record phases[14][15]. Restless Legs Syndrome (RLS)[16] Leg paresthesias, worse at rest/night, relieved by movement[16][17]. Basal ganglia dopamine dysfunction[17]. Tx: Dopamine agonists (ropinirole), gabapentin[17]. Degenerative Neurologic Disorders[1] Multiple Sclerosis (MS): Autoimmune T-cell CNS demyelination[18][19]. Signs: optic neuritis, spasticity, ataxia, bladder dysfunction[20][21]. Tx: DMDs (interferons)[22], steroids for relapses[22]. Parkinson's (PD): Substantia nigra DA neuron loss; DA/ACh imbalance[23]. Key: resting tremor ("pill-rolling"), cogwheel rigidity, bradykinesia (masked facies, shuffling gait), postural instability[23]. Tx: Levodopa/Carbidopa (avoid protein meals[26]), DA agonists, DBS[25]. Myasthenia Gravis (MG): Autoimmune AChR antibody destruction[29]. Fluctuating weakness (ptosis/diplopia; worsens with activity, improves with rest)[29]. Dx: Edrophonium test (atropine bedside)[30].Myasthenic Crisis: Respiratory failure[30]; Tx: IVIG, plasmapheresis[31]. Cholinergic Crisis: Excess anticholinestase[30]; SLUDGE signs[30]; Tx: hold drugs, atropine[30]. Tx: Pyridostigmine[30]. Amyotrophic Lateral Sclerosis (ALS): Upper/lower motor neuron degeneration; cognition spared[32][33]. Wasting, bulbar signs. Death: respiratory failure[32]. Tx: Riluzole[32]. Huntington's (HD): Autosomal dominant CAG repeats[33]. ACh/GABA deficit, excess DA[33]. Key: chorea, psychiatric decline, dementia[33][34]. Caloric needs: 4000-5000 kcal/day[34]. Tx: Tetrabenazine[34].

CC CJM | Burns

Burn Classification & TBSA Assessment Burn severity depends on depth, extent (TBSA), location, and patient risk factors[1]. Depth is classified as partial-thickness (epidermal/dermal; painful, red, blistered) or full-thickness (dermal destruction, painless, leathery eschar, visible thrombosed vessels)[2]. TBSA is estimated using the Rule of Nines for adults or the Lund-Browder chart for children[6]. Referral to a burn center is indicated for partial-thickness burns >10% TBSA, chemical/electrical burns, inhalation injury, or burns of the face, hands, feet, genitalia, perineum, or joints[7]. Face, neck, and circumferential torso burns threaten ventilation[8]. Circumferential limb burns impair perfusion, requiring escharotomy[8][9]. Emergent Phase Pathophysiology & Resuscitation The emergent phase (first 72 hours) prioritizes burn shock and gas exchange[10]. Loss of capillary seal triggers a massive fluid shift from the intravascular to the interstitial space (third spacing), causing severe hypovolemia, hemoconcentration, high blood viscosity, and increased peripheral resistance[10]. Damaged cells release potassium (hyperkalemia), and sodium moves into the interstitium (hyponatremia)[13][14]. Inhalation injuries (carbon monoxide, above/below glottis) cause mucosal edema, obstruction, and pneumonia (the leading cause of death)[9]. Myoglobinuria (from electrical muscle damage) can block renal tubules, causing acute kidney injury (AKI)[18][19]. Priority care includes early intubation, 100% humidified O2, and resuscitation[20][21]. The ABA formula dictates 2–4 mL Lactated Ringer's per kg per % TBSA in the first 24 hours (half in the first 8 hours)[22]. Target clinical parameters are MAP >65 mmHg, HR <120 bpm, and adult urine output of 0.5–1 mL/kg/hr (75–100 mL/hr for electrical burns)[25]. Acute, Rehabilitative & Psychosocial Care The acute phase begins with diuresis and ends when wounds are nearly healed[26]. Sepsis, often from gram-negative bacteria or Candida, is a leading cause of death during this immunosuppressed period[27][28]. Stress-induced hypermetabolism causes protein catabolism and transient hyperglycemia, requiring early enteral nutrition and insulin[29]. Excision and grafting (autograft, CEA, or Integra) are vital for full-thickness wounds[32]. Pain is managed with continuous IV opioids, procedural breakthrough doses, and anxiolytics[36][37]. Continuous physical therapy and splinting prevent contractures[38][39]. In the rehabilitation phase, hypertrophic scars are minimized using custom-fitted pressure garments worn up to 23 hours daily for 12–18 months[40][41]. Hydration and antihistamines help relieve severe itching[40][42]. Older adults face higher mortality due to thinner skin, delayed healing, and co-morbidities[43]. Support groups and psychiatric interventions address emotional needs, body image changes, and PTSD[44].

CC CJM | Intro

the intro episode to the clinical judgement model

27 di 34