400 likes | 531 Views
Program Information. Critical Temperature-Related Illnesses. Dorothy W. Bird, MD Suresh Agarwal, MD Department of Surgery Boston University Medical Center. Temperature-Related Illness. Hypothermia Systemic Hypothermia Non-freezing Injuries Freezing Injuries Hyperthermia
E N D
Critical Temperature-Related Illnesses Dorothy W. Bird, MD Suresh Agarwal, MD Department of Surgery Boston University Medical Center
Temperature-Related Illness Hypothermia Systemic Hypothermia Non-freezing Injuries Freezing Injuries Hyperthermia Heat Exhaustion Heat Stroke Drug-Induced Hyperthermia
Heat Exchange Mechanisms Radiation: loss of heat by infrared rays Conduction: transfer of heat from object to object Convection: current of air carrying heat away from skin Evaporation: warming of water to transform it from liquid to gas
Normal Temperature Regulation Human body generates 1oC/hour Transfers heat to the environment to maintain body temperature +/- 0.6oC Normal body temperatures: 32oC skin 37oC sublingual 38oC rectum 38.5oC deep liver
Hypothermia <35oC (95oF) Primary (accidental): decrease in core body temperature from environmental cold stress Secondary: due to metabolic disorder resulting in abnormal heat production or heat-conserving mechanism
Hypothermia - Systemic Effects A. Cardiovascular Delayed bradycardia (32oC) ↓MAP, ↓contractility, ↓CO EKG: J-wave, PR, QRS, QT prolongation 30oC atrial or ventricular fibrillation 25oC asystole B. Respiratory ↓RR, hypoxia, respiratory acidosis ↑mucus (cold bronchorrhea) ↓ciliary action, ↓cough reflex; pneumonia
J-Wave http://www.rcsed.ac.uk/fellows/bcpaterson/new_page_3.htm
Hypothermia – Systemic Effects C. CNS Abnormal EEG <34oC; Flat EEG 19-29oC Hyper-reflexia >32oC; Hypo-reflexia <32oC ↓Mentation, ↓Motor function D. Coagulation Platelet sequestration (portal), thrombocytopenia Impaired platelet function Coagulation factors: ↓40% activity, ↑PT, PTT DIC-like syndrome, risk of thromboembolic event
Hypothermia – Systemic Effects E. Renal ↓Na+ reabsorption F. GI Ileus, bowel wall edema, impaired hepatic drug detoxification, pancreatitis, hyperamylasemia, gastric erosions
Hypothermia – Systemic Effects G. Endocrine Hyperglycemia H. Immune ↓endothelial cell adhesion results in ↑infection
Hypothermia - Management ABCs first! May be hard to palpate pulse/BP in cold, stiff victim EKG: look for any organized rhythm as evidence of life CPR ONLY in absence of cardiac rhythm NO cardiac drugs or defibrillation <28oC
Hypothermia - Rewarming Mild Hypothermia (32-35oC) Warm environment – blanket, head cover Moderate Hypothermia (30-32oC) Heating pad, warm water immersion Severe Hypothermia (<30oC) Warm IV fluids (65oC) / blood products (49oC) Cardiopulmonary bypass Lavage
Re-warming Rates Spontaneous: 1.2oC/h Spontaneous + Shivering: 3.6oC/h Passive External Rewarming: 0.5-2.0oC/h Active External Rewarming: 1.0-2.5oC/h Body Cavity Lavage: 1.0-3.0oC/hour Cardiopulmnary Bypass: 1.0-2.0oC/3-5min CAVR: 1oC/15.4 min
CAVR Continuous arteriovenous re-warming Level I warming system Percutaneous femoral arterial and venous lines Creates AV fistula where blood is pumped via patient’s own BP through external warming system More rapid re-warming than other methods Less invasive, no heparinization needed Improved survival, multisystem organ failure, SICU stay vs other methods
Hypothermia in Trauma Very common after injury A form of secondary, unintentional hypothemia Ominous sign!! Worsened outcome / mortality if due to trauma ↑ mortality if patient controlled for ISS, shock, resuscitation volume
Hypothermia in Trauma Stricter Severity Classification: Mild: 36-34oC Moderate: 34-32oC Severe: <32oC Rapid re-warming with CAVR proven more effective Failure to re-warm is detrimental to survival!
Non-freezing Injury Chilblain (Pernio) Cause: Repeated exposure to cold above freezing Pathophysiology: chronic dermal vasculitis Appearance: pruritic, red-purple papules, maculares, plaques, nodules, edema, blisters Treatment: shelter, elevation on sheepskin, gradual rewarming at room temperature Sequelae: dermopathy; treat with antiadrenergic (prazosin) or calcium-channel blocker (nifedipine)
www.answers.com/topic/chilblain www.ohiohealth.com/bodymayo.cfm?xyzpdqabc=0... Chilblain
Non-freezing Injury Trench foot (hand) Cause: chronic exposure to wet conditions just above freezing Pathophysiology: alternating arterial vasospasm and vasodilation Appearance: edema, blisters, redness, ecchymosis, ulceration Treatment: removal from cold, wet environment; gentle warm, dry air; elevation; wound care Sequelae: cellulitis, lymphangitis, gangrene, demyelation, atrophy, osteoporosis, fallen arches
Trench Foot • www.visualstatistics.net • www.pbase.com
Frostbite Freezing injury: Ice crystal formation, cellular dehydration, microvascular occlusion Pathophysiology: 1. cellular death from freezing cold 2. alternating vasoconstriction/vasodilation (Hunting reaction)→ repeat freeze/thaw cycle→ ↑blood viscocity→ progressive thrombosis→ ischemia/necrosis 3. re-warming→ secondary ischemia/reperfusion
Frostbite Classification: 1st Degree: tissue freezing, central white anesthetic patch, surrounding erythema 2nd Degree: tissue freezing, blisters of clear or milky fluid, surrounding edema/erythema 3rd Degree: tissue freezing and subcutaneous/skin death, hemorrhagic blisters, black eschar (2 weeks) 4th Degree: tissue necrosis, gangrene, full-thickness tissue loss; hard, cold white, anesthetic
Frostbite • www.geradts.com • www.alpineinstitute.blogspot.com
Frostbite Treatment 1. Pre-thaw/Pre-hospital Phase Protect injured limb from trauma No thawing until definitive re-warming is ensured NO rubbing!
Frostbite 2. Re-warming/Hospital Phase Rapid re-warming: immersion in large water bath (40-42oC) x30-45 minutes Narcotic pain relief as needed 3. Post-thaw Phase Wound care: clean and dry skin, elevate, sterile cotton applied between affected toes/fingers, protect from unintentional trauma with tent/cradle
Frostbite Wound Care Uninfected blebs: keep intact (self-dressing) Daily or BID dressing change/cleansing in warm whirlpool bath Aloe vera cream (thromboxane inhibitor) Physical therapy with edema resolves No tobacco, nicotine, vasoconstrictors
Frostbite Sequelae Cold insensitivity Hyperhidrosis Neuropathy ↓ nail/hair growth Persistent Raynaud’s phenomenon ↑ risk for re-injury
Hyperthemia Hyperthemia vs. Fever: elevated body temperature Hyperthermia: abnormal temperature regulation Fever: normal temperature regulation with elevated set-point Hyperpyrexia: extreme temperature elevation (>40oC)
Heat Exhaustion Heat exposure resulting in volume depletion Flu-like symptoms: Hyperthermia(>36oC), muscle cramps, nausea, malaise, tachycardia Hypernatremia (sweating)/Hyponatremia ( excessive water consumption) No neurologic impairment Treatment: volume/electrolyte repletion
Heat Stroke Extremely elevated body temp (>41oC) Neurologic dysfunction Severe volume depletion, hypotensive, multiorgan failure, rhabodmyolysis, acute renal failure, DIC, transaminitits Anhidrosis Classic Type Exertional Type
Heat Stroke Treatment Volume and electrolyte repletion Immediate cooling External cooling: ice pack to groin, axilla, ice to neck, chest; cooling blankets Evaporative cooling: spray skin with cool water and fan; will decrease temp by 0.3oC/min Internal cooling: cold water lavage to stomach, bladder, rectum
Drug-Induced Hyperthermia Malignant Hyperthermia (MH) Excessive calcium efflux from sarcoplasmic reticulum in response to halogenated inhalational agents Results in uncoupling of oxidative phosphorylation with dramatically increased metabolic rate Incidence: 1:15,000 episodes of general anesthesia Affects 1:50,000 people Autosomal dominant inheritence
Malignant Hyperthermia Signs FIRST: sudden rise in end-tidal CO2 Muscle rigidity Hyperthermia Depressed consciousness Autonomic instability Leads to: myonecrosis, rhabdomyolysis, acute renal failure
Malignant Hyperthermia Management Discontinue anesthetic agent DANTROLENE- blocks Ca++ efflux from S.R. First: 1-2mg/kg IV bolus q15 min to max total 10mg/kg Then: 1mg/kg IV (or 2mg/kg PO) QID x 3 days Reduces mortality from 70% to 10% Victims should wear ID band and family should be tested
Neuroleptic Malignant Syndrome Idiosyncratic drug reaction to usage or discontinuation of neuroleptic drugs that alter dopamine axis Symptoms: hyperthermia, lead-pipe rigidity, altered mental status, autonomic instability 20% mortality 0.2%-1.9% incidence (of those on neuroleptics) Most common: Haloperidol, Fluphenazine No relationship to duration or dosage Usually seen 24-72 hours after starting/ending drug
NMS Treatment Discontinue offending new medication or resume dopaninergic therapy if recently stopped Volume resuscitation DANTROLENE: 2-3mg/kg/ IV q few hours to max total 10mg/kg/day BROMOCRIPTINE: 2.5-10mg PO TID Give with heparinization due to increased thromboembolism risk
Serotonin Syndrome (SS) Caused by overstimulation of serotonin receptors in CNS Associated with SSRI, NMDA, amphetamine use Exam: abrupt onset of altered mental status Autonomic hyperactivity Mydriasis, diaphoresis Tachycardia, hypertension Hyperthermia Hyperkinesia, ↑DTR, rigidity, clonus (deep patellar, horizontal occular clonus)
Serotonin Syndrome Treatment Discontinue medication Benzodiazepine (control agitation, hyperkinesia) Cyproheptadine (serotonin agonist) Only for severe SS Give 12mg PO/NG then 2mg PO q2h PRN symptoms Neuromuscular paralysis (Vecuronium) NO RESTRAINTS
References Jurkovich GJ. Environmental Cold-Induced Injury. Surg Clin N Am 2007;87(4):247-267. Petrone P, Kuncir EJ, Asensio JA. Surgical management and stratagies in the treatment of hypothermia and cold injury. Emerg Med Clin N Am 2003;21:1165-1178. Hall JB, Schmidt GA, Wood LDH. Principles of Critical Care 3rd Ed. The McGraw-Hill Companies, 2005. Marino PL. The ICU Book, 3rd ed. New York: Lippincott Williams & Wilkins, 2007:697-712.