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PGY1 Environmental Injuries Block > Disaster > Flashcards

Flashcards in Disaster Deck (111):

factors that indicate an increasing probability of mass casualty incident

terrorist activity, increasing population density in floodplains, seismic zones and areas susceptible to hurries, production and transport of thousand of toxic and hazardous materials, risk associated with fixed-sitenuclear and chemical facilities, possibility of catastrophic fires and explosions and climate change


what are the 3 basic components of surge capacity

staff (hospital personnel)
stuff (supplies and pharmaceuticals)
structure (physical location and management infrastructure)


what is surge capacity

situation where demand exceeds available resources


define disaster

an event which overwhelms response capabilities


how to define a potential injury creating event (PICE)

A: static vs. dynamic (is there potential for more victims)
B: controlled, disruptive, paralytic (need of more resources - no, augmentation, and total reconstitution)
C: local, regional, national, international

Projected Need
0 - None
I- Small
II- Moderate
III- Large


six critical substrates for hospital operations

physical plant
supplies and equipment
supervisory managerial support


how is triage different in disaster ?

attempts to do the most good for the most people, if patient does not have respirations after repositioning airway, should move on to next


which groups o people are at greater risk for injuryy, death, and property loss resulting from a disaster

racial and ethnic minorities
those siding in institituoins
mentally ill


components and roles of incident command system

incident commander: overall mgmt responsibility for incident
operations section: mgmt of tactical activities, resources assigned to staging areas
planning section: collects, evaluations and disseminates info about incident operations and status of resources
logistics section: providing facilities, services and material in support of the incident (i.e. food, medical support, transportation)
finance section: maintaining records on personnel and equipment, paying vendors/supplies, determingin cost of alternative of strategic planning


4 phases of comprehensive emergency management

mitigation: taking action to reduce impact of identified hazards, i.e enhanced seismec structural design of hospital
preparedness: training, drills and cataloging of resources
response: assessment of situation and coordination of resources
recovery: return to normal operations and debriefing to critique response


potential agents of high concern for use as weapons of mass destruction

chemical: nerve agents: sarin, soman, tabun, VX; mustard agent

biologic: anthrax, plague, smallpox, botulism, viral hemorrhagic fever, tularemia

radiologic: simple device, dispersal device


clinical features of patient exposed to radiation (WMD)

symptoms within hours to days
dermal burns, bone marrow failure, GI dysfunction


3 types of radiation exposure

irradiation, internal contamination, and external contamination


which type of radiation exposure poses no threat to ED personnel


same as getting a CXR


management of internally contaminated radiation patient

isolation room where all secretions and body fluids can be collected

agents to limit uptake or facilitate removal of certain radioactive substances:
Prussian blue for caesium/thallium ingestions
diethylenetraiminepentaacetic acid (DTPA) for plutonium exposure


management of external contaminated radiation patient

removal and clothing and washing with soap and water
washing by protected personal should continue until monitoring by the radiation safety officer demonstrates the absence of radioactivity

if wounds present, decontaminate these first, then cover with sterile ,waterproof dressing, then remaining skin washed

ideally decontaminate before hospital entry


features of weapons of mass destruction threat

fear of unknown or unfailiar
lack of training for hospital personnel
lack of equipment, including PPE and diagnostic aids
potential for mass casualties
psychological cassaties
crime scene requiring evidence collection and interaction with law enforcement
potential for ongoing morbidity and mortality (dynamic situation)


signs suggesting biological weapon deployment

syndromes: pulmonary symptoms, pneumonia, rashes, sepsis syndrome, influenza symptoms
epidemiology: multiple, simultaneous events, dead animals, large numbers of patients with high toxicity and death rate


three groups of biologic weapons

bacteria, viruses and toxins


recommendations for prevention of in-hospital transmission of contagious agents

isolate patient in single room with adjoining anteroom
have hand washing facilities and PPE in anteroom
use negative air pressure if possible
use strict barrier precautions: PPE, gowns, gloves, high efficiency particulate air (HEPA) filter respirators, shoe covers, protective eye wear
alert hospital departments that generate aerosols : lab (centrifuges), pathology (autopsies)


what is anthrax / how spread

Bacillus anthracis, a gram positive spore-forming bacterium -- spores cause disease

inhaled spores, etc.
no human to human


clinical manifesations of anthrax infection

influenza like illness, with malaise, fever and nonproductive cough with 2-10 days of exposure to spores

within 24-48 hours of illness, abrupt deterioration occurs with overwhelming sepsis, shock, hemorrhagic mediasitnitis, dyspnea and stridor


what is clinical course of cutaneous anthrax

spores introduced through skin usually through open wounds or abrasions; mortality rate 20% without tx, 1% with treatment
papule develops in 1-5 days and progresses to form a large vesicle, then severe edema around the lesions with regional lymphadenitis
after 1 week lesion ruptures forming a black eschar
in 2-3 weeks it sloughs off and illness is over or organism disseminates and pt dies


presentation of oropharyngeal anthrax

ingestion of contaminated meat, pt develops sore throat and neck swelling from cervical and submandibular lymphadenitis
dysphagia and resp distress develop


presentation of GI anthrax

ingestion of contaminated meat, N/V and fever with mesenteric lymphadenitis
pt then experience severe abdominal pain, hematemesis, ascites, and bloody diarrhea


treatment of anthrax - cutaneous anthrax without toxicity

cipro 500mg po Bid or doxycycline 100mg po bid, or amoxicillin 500mg PO TID x 7-10 days


treatment of inhalation, cutaneous, or GI anthrax WITH toxicity

cipro 400mg IV q12h or doxycyclin 100mg IV q12h, or penicillin G 4 million units IV q4h

PLUS clindamycin or linezolid

if meningitis ADD drug that penetrates CNS - meropenem


treatment of post exposure prophylaxis for anthrax

cipro 500mg po Bid or doxycycline 100mg po bid, or amoxicillin 500mg PO TID
treat for 60 days or until patient receives three doses of vaccine


what is the plague caused by

Yersinia pestis a gram negative bacillus
disease of rodents transmitted to humans by flea or inhalation


what are the 3 forms of the plague

bubonic, septicemic, pneumonic


clinical features of pneumonic plague

incubation of 2-3 days
sudden onset of fever, chills and flu-like illness
within 24 hours fulminant pneumonia associated with hemoptysis, systemic toxicity, respiratory failure, circulatory collapse, and death

ecchymoses, DIC and aural gangrene (black death)

human to human transmission possible with pneumonic plague only


clinical features of bubonic plague

organisms inoculated into skin, usually from flea bite
2-3 day incubation, bacilli migrate to lymph nodes and cause inflammation/necrosis, causing large tender nodes or buboes

half will become disseminated


treatment of plague

pneumonic isolation x 4 days
bubonic/septicemic isolation x 48 hours

streptomycin 1g IM BID, gentamicin 5mg/kg once daily IM or IV, doxycycline 100mg IV BID, ciprofloxacin 400mg IV BID, chloramphenicol 25mg/kg IV QID for minimum 10 days

OR doxyclycline 100mg BID, copra 500mg Bid, or chloramphenicol 25mg/kg QID


prophylaxis medications for the plague

tetracycline, doxycycline, cirpro, chloramphenicol and possible septra for kids


how is smallpox spread

variola virus, spread as aerosol, can survive 24-48 hours in environment

people infectious from time rash first appears until scabs fall off (1-2 weeks)


clinical course of smallpox

virus inhaled
migrates to regional lymph nodes, replicates for 2-4 days then spreads to spleen, bone marrow and other lymphoid tissue and liver
8-12 days fever, prostration and headache, mental status changes can occur
rash appears first on face and forearms, later spreading to legs and trunk
all lesions at same stage in one area of the body
during next 8-14 days pustules crust over and separate from the skin, leaving pitted scars


major criteria for diagnosis of smallpox

3 major:
febrile prodrome
classic smallpox lesions
lesions in small stage of development

5 minor:
centrifugal distribution of pustules
first lesions on the oral mucosa, face or forearms
toxic appearnce
slow evolution of lesions
pustules on palms and soles


treatment of smallpox

cidofovir in animal trial showed 100% survival

vaccinia immune globulin - no role in active disease, can give within 3 days of exposure to prevent or ameliorate illness, within 7 days may prevent death


emergency department preparedness for chemical weapons of mass destruction

community-based hospital planning
personnel trained in recognition, mass casualty triage and treatment
decontamination facility with protocols (runoff water, warm water)
PPE readily accessible and compliant with regulations
rapid access to antidotes, cyanide kits, and anticonvulsants
hospital incident management system in place
knowledge of how to access experts quickly


4 classes of chemical compounds used as WMDs

nerve agents
vesicants (blistering)
pulmonary intoxicants


how does nerve agents work

inhibit AChE, block degradation of ACh at postsynaptic membrane

cholinergic toxidrome - most worrisome symptoms bronchorrhea and bronchoconstriction
mitosis and fasciculations occur

bradycardia rare with nerve agents unlike other organophosphate


symptom onset after exposure to nerve agentss

seconds after inhalation and peak at 5 mins

if patient asymptomatic after 1 hour they have not received clinically significant exposure


treatment of nerve agent exposure

mild: observe for 1 hour, then release
moderate: one or two Mark I kits IM or atropine 2-4mg IV, may repeat q5-10mins pen and 2-PAM 1g IV during 20 mins, may repeat q1h
severe: three Mark I kits IM and one diazepam auto injector IM; or atropine 6mg IV, may repeat 2mg boluses IV q5-10mins, and 2-PAM g IV during 30 mins,

mild: one Mark I kit, or atropine 2mg IV and 2PAM 1gIV
mod/sevre: same as for vapor


symptoms by mild, moderate severe after vapour exposure to nerve gas Sarin

mild: rhinorrhea and mitosis
moderate: mild sx. plus increased secretions, wheezing/dyspnea, muscle weakness or fasciculations or GI effects
severe: apnea, seizures, LOC, flaccid paralysis, or major involvement of 2 organ systemns


symptoms by mild, moderate, severe after liquid exposure to nerve agent VX

mild: localized sweating and fasciculations where a drop touches skin, no miosis (may be delayed for 18h)
moderate: GI effects, mitosis uncommon (may be delayed for 18h)
severe: apnea, seizures, LOC, flaccid paralysis, or major involvement of two organ systems occurs in less than 30 minutes at or above median lethal dose


clinical presentation of mustard injury

skin blisters resembling second degree burns

airway injury ranging from irrigation to nose, sinuses, and pharynx to hemorrhagic necrosis of bronchioles


treatment of mustard injury

eyes: irrigation, mydriatics, topical abx, petroleum jelly to lids to prevent adhesions
burns: decontamainte skin, with water
airway injury: mild- cool humidified mist, moderate- O2, CPAP or intubation, severe- intubation, inline bronchodilators, PEEP


how does cyanide work

bind to cytochromes within mitochrondria and inhibit cellular oxygen use


clinical features of CN

tachypnea, h/a, dizziness, vomiting, anxiety
at higher doses, seizures, respiratory arrest, and systole within minutes


tx of CN poisoning

IV hydroxycobalamin 5g


what is aging in terms of organophosphate pesticides

irreversible conformational change that occurs when organophosphate is bound to cholinesterase enzyme for a prolonged time - causes clinical effects to persist for days to weeks


clinical features of organophosphate toxicity

muscarinic ACh: salivation, lacrimation, urinary incontinence, defecation, emesis, bronchospasm, bronchorrhea, and bradycardia

nicotinic ACh: tachycardia, tachydysrhythmias, and skeletal muscle fasciculations

at the NMJ: weakness, fasciculations, paralysis --- excessive ACh causes hyper stimulation of muscles with secondary paralysis; when diaphragm affected causes respiratory arrest

sympathetic stimulation: diaphoresis, htn, tachycardia, mydriasis

sympathetic stim + NMDA effects: seizures

pulmonary edema


DDX of acetylcholinesterase inhibitor poisoning

carbamate pesticides
carbamate medications (ie. rivastigmine)
nicotine and other nicotine alkaloids and cholinomimetics such as pilocarpine

inferior wall MI causing exaggerated vagal response
exaggerated sympathetic responses, ie. thyroid storm, pheochromocytoma


treatment of organophosphate poisoning

1. decontamination: flush skin with water, remove clothing; if ingestion no role for GI decontamination as rapidly absorbed
2. supportive care with emphasis on respiratory stablization
3. reversal of ACh excess : atropine
4. reversal of toxin binding at receptor sites on cholinesterase molecule : 2-PAM


indications for pralidoxime in organophosphate poisoning

resp depression or failure
muscle fasciculations
hemodynamic instabilty
use of large amounts or repeated doses of atropine to completely control signs and symptoms of OP intoxication


what are examples of simple asphyxiants and how do they produce toxicity

inert gases which produce toxicity only by displacement of oxygen and lowering FiO2
ex: CO, CO2, N2, CH4, NO, He & other noble gases

its have rapid resolution on removal from exposure


diagnostic tests after exposure to simple asphyxiant gas

if minimally symptomatic, CXR or ABG not required
tox testing only needed if apshyxiation was an act of deliberate self harm


disposition of patients exposed to simple asphyxiant

mild asphyxia who recover after removal from exposure can be D/C'd after 6 hours of observation if asymptomatic or minimally symptomatic and improving

patients at risk for complications of hypoxia, i.e. those presenting with coma, chest pain, ECG changes or with exacerbating medical conditions (cardiac disease), observed for 24-48 hours for development or progression of post-hypoxic complications


how do irritant gases produce toxicity and examples

dissolve in respiratory tract mucus and alter air-lung interface by invoking an irritant or inflammatory response

ex: acrolein, ammonia, chloramine, chlorine, HCl, HF, oxides of nitrogen, oxygen, ozone, phosgene, sulfur dioxide


what determines the effect of pulmonary irritant gases

water solubility
highly soluble rapidly impact mucous membranes o eyes and upper airway; massive or prolonged exposure can result in life-threatening laryngeal edema, laryngospasm, bronchospasm, or ARDS

poorly water soluble do not irritate at low concentrations and some have pleasant odors so prolonged breathing in toxic environment allows time to reach deep into alveoli - can see delayed irritation 2-24 hours after exposure


management/disposition of patients exposed to pulmonary irritants

pt with no upper airway symptoms, normal voice, and no evidence of irritation (erythema) on exam of oral pharynx require no further upper airway evaluation but should be re-examined if symptoms or signs develop later

if exposed to intermediate or poorlywater soluble gas - observe for 6 hours

if prolonged exposure, or exposure to highly concentrated gases in closed space or high-risk (underlying pulmonary disease ,extreme of age, poor f/u), observed for 24 hours

pt with evidence of severe tissue irritation such as oral or tongue edema, altered voice (raspy or muffled), or significant odynophagia or dysphagia should undergo early intubation because progression can be expected

pt with significant erythema or pain in the oropharynx or nasopharynx and those with any evidence of alteration of voice, dysphagia or odynophagia, or stridor require early exam by laryngoscopy (with appropriate sedation/topical anesthesia) -- laryngoscopy guides decision to intubate


treatment for patients exposed to chlorine or HCl gas

nebulizer 2% NaHCO3 - symptomatic relief


what does metabolic acidosis, particularly when serum lactate greater than 10mmol/L suggest in inhalation injury post fire

cyanide poisoning


diagnostic testing of smoke inhalation pt

airway patency assessed early
if carbonaceous sputum or hoarse voice, assess airway with laryngoscopy, and secure airway if signs of injury or compromise noted

assess pulmonary injury with ausculation/ CXR

VBG, COHb, methemoglobin level


how do cyanide and hydrogen sulfide produce toxicityq

inhibits oxidative metabolism for by binding to cytochrome c oxidase of ETC in mitochondria


rapid CV collapse, hypotension, bradycardia, ventricular dysrhythmias and seizures in fire victim should suggest _____

cyanide poisoning ,severe CO poisoning or both


treatment of cyanide poisoning

adults 5g over 15 mins

cyanide antidote kit:
1. MetHb inducers: amyl nitrite or NaNO2 10mL 3% solution IV over 2-4 mins
2. cyanide detoxification
Na-thiosulfate 25% solution IV- 50mL adult


effects of using hydroxocobalamin

hypertension in those not cyanide poisoned
bright red discolouration of patient skin

interferes with lab tests of COHb, possibly serum lactate so check these before its given


when to not use cyanide antidote kit

fire victims with concomitant CO poisoning because methemoglobin +COHb = less O2 delivery to tissues


clinical features of CO poisoning

altered mental status, extremely abnormal vitals including hypotension and cardiac arrest, h/a, N/V, dizziness, myalgia, and confusion


recommendations for hyperbaric O2

COHb - > 25% with no clinical findings, >15% in pregnancy or fetal distress

or an elevated COHb with one of the following: syncope, coma, seizure, AMS/confusion, abnormal cerebellar function, prolonged CO exposure with minor clinical findings


3 burn zones described by Jackson

central zone of irreversible necrosis
intermediate and potentially reversible zone of stasis
outermost reversible zone of inflammation


features of 1st degree burn

appearance: red, no blisters
blanches with pressure: yes
sensitivity to pinprick: very
pliability: soft
time to healing: 1 week
need for excision and grafting: no


features of superficial partial thickness (second degree)

appearance: red, blisters
blanches with pressure: yes
sensitivity to pinprick: very
pliability: soft
time to healing: 1-2 weeks
need for excision and grafting: no


features of deep partial thickness (second degree) burn

appearance: red or white, no blisters
blanches with pressure: maybe
sensitivity to pinprick: yes
pliability: slightly tense
time to healing: 2-3 weeks
need for excision and grafting: yes


features of full thickness (third degree) burns

appearance: leather like, charred
blanches with pressure: no
sensitivity to pinprick: no
pliability: stiff, leather like
time to healing: >3 weeks
need for excision and grafting: yes


how to calculate TBSA in burns

rule of nines: head-9, entire arm-9, front of trunk - 18, back of trunk- 18, upper leg- 9, lower leg- 9, perineum- 1, palm-1
kids: Lund-Browder chart accounts for age related differences


what %TBSA is defined as mild (by age group) and what is their disposition

children- <5% TBSA
adult - <10% TBSA
elderly- <5% TBSA
all- <2% full thickness

outpatient mgmt


what %TBSA is defined as moderate (by age group) and what is their disposition

children - 5-10% TBSA
adult - 10-20% TBSA
elderly- 5-10% TBSA
all- 2-5% full thickness, high voltage, inhalation, circumferential, comorbid disease



what %TBSA is defined as severe (by age group) and wha tis their dispositon

children - > 10% TBSA
adult- >20% TBSA
elderly- >10% TBSA
all- >5% full thickness, high voltage, significant burn to face, eyes, ear, genitals or joints, or significant associated trauma

burn unit


DDX for burns

toxic epidermal necrolysis/Steven-JOhnson syndrome


lab tests for suspected inhalation injury

VBG - including CO levels


lab tests for burn victims

if they require admission: CBC, lytes, Cr, type and cross, coags


initial first aid of burns

cool burns with room temp water
remove pt from source of injury/ any garments or jewelry should be removed
with large burns watch for hypothermia
leave blisters in tact unless very tense/large or over joints

2 large bore IVs, fluid ressus started
O2 to maintain above 92


clinical signs to suggest inhalational injury

facial burns
carbonaceous sputum
singed nasal hairs


who needs intubation post- fire / how to manage airway

signs of inhalational injury

best way to confirm inhalation injury is with direct visualization with fiberoptic, video, or direct laryngoscopy using topical anesthesia with mild/moderate sedation prn (ie. 10-20mg ketamine)
presence of soot or significant deem in supraglottic region means immediate intubation

avoid RSI unless direct confirms easy airway
awake intubation when difficult suspected


indications for ETT and MV

upper airway obstruction
inability to handle secretions
hypoxemia despite 100% O2
patient obtundation
muscle fatigue suggested by high or low RR
hypoventilation (PCO2 > 50, pH <7.2)


fluid resus formula in burns

Parkland- 4cc/kg/%TBSA of RL over 24 hours, half in first 8 hours, other half in 16 hours

modified Brooke- 2cc/kg/%TBSA of RL in adults, and 3cc/kg/%TBSA in kids


what burn sites may require escharotomy

circumferential around thorax may impede ventilation
circumferential around limbs may impair circulation/lead to compartment syndrome


signs/symptoms pt may need escharotomy

absence of distal pulses/distal Doppler and pulse oximetry
increased pain, especially with passive motion, allow, weakness and sensory loss may be signs of impending compartment syndrome


local wound therapy for burns

1st degree- topical NSAID/aloe vera, PO NSAIDs

clean burn with soap and water
aspirate with needle or de-roof large tense blisters - if pt being transferred cover burn with clean, nonadherent dressing

topical antibacterial ointment + non-occlusive dressing maintains moist environment and do not adhere to overlying dressings
silver dressings better than silver sulfadiazine

topical agents should be applied once or twice daily after washing burn with mild soap and water while removing any non-adherent debris

Mepilex Ag - occlusive dressing works well for exudative dressing, don't need to change as much - can be left for 1 week


criteria for referral to a burn center

partial thickness burns > 10%
burns that involve face, hands, genitals, perineum or major joints
3rd degree burns in any age
electrical burns, including lightning
chemical burns
inhalation injury
burn injury in pts with preexisting medical disorders than could complicate mgmt, prolong recovery, or affect mortality
any patients with burns + trauma where burn causes greatest risk of morbitiy/mortality
burned kids in hospitals that don't have supplies/personnel to deal with kids
burn injury in patients who will require special social, emotional or rehab


What are the 4 measures of radiation

Radioactivity: amount of ionizing radiation released by a material
Exposure: amount of radiation traveling through air
Absorbed dose: amount of radiation absorbed by a person
Dose equivalent: combines amount of radiation absorbed with the tissue damaging potential of the type of radiation


What are the 3 ways one can be exposed to radiation

Irradiation: object or person exposed to radioactive source
Incorporation: radioactive material taken up by tissue cell or organ ( ingestion, inhalation, or absoprtion via open wound)
Contamination: exposure to radioactive particulate matter (externally or if inhaled and deposited into lungs)


What are the 3 phases of acute radiation syndrome and what characterizes the phases

Prodromal phase: nonspecific symptoms (anorexia, N/V, fatigue)
Latent phase: initial symptom improvement
Manifest illness phase: neurovascular syndrome onset, GI syndrome onset, hematopoietic syndrome onset


What does early onset nausea and vomiting indicate after radiation injury

Severe radiation injury


What is the first cell line to deplete in radiation illness



What are the symptoms in GI subset of radiation illness

N/v, GI bleeding, malabsorption, and massive fluid loss leading to hypovolemia and CV collapse- symptoms due to death of intestinal epithelial precursor cells


What symptoms are associated with neurovascular sub syndrome of radiation sickness

Irritability, altered mental status, seizures, prostration, ataxia, hypotension


Diagnostic test in radiation injury

Contamination survey instrument - Geiger muller detector
CBC q6h
Lipase, lfts, CRP


How to decontaminate radiation injury patient

Remove clothing
Soap and water exposed skin
Collect all wash water and mark as radioactive waste
High pressure irrigation of wounds


Indication for cytokine therapy (CSF) in radiation injuries

Greater than 2Gy dose, decrease in lymphocyte count, and if leukopenia expected to last more than 7 days


How to use CSF / cytokines in radiation injury

Start within 24 hours and continue until absolute lymphocyte count above 1000


What is the most important prognostic indicator in radarionnexposure patients

48 hour absolute lymphocyte count


4 basic pathophysiologic processes in rhabdomyolysis

1. impairment of muscle production or use of ATP, [ATP] in cell falls, disrupts chemical gradients due to failure or Na-K-ATPase, leads to cell membrane and sarcolemma compromises and cell destruction
2. disruption of delivery of O2, glucose, and other nutrients to skeletal muscle
3. increases in metabolic demands beyond ability of organism to deliver O2 and nutrients
4. direct myocyte damage


causes of rhabdomyolysis

prolonged immobilization (due to pressure on gravity-dependent body parts)
excessive muscle activity
muscle ischemia -ie. arterial occlusion, CO posiongin, external compression/crush
temp extremes - sarcolemma disruption, ie. heat stroke, NMS, MH, and hypothermia
electrical current - sarcolemma directly injured
electrolyte abnormalities - hypokalemia (low K leads to focal muscle vasoconstriction and ischemia), hypophosphatemia (not enough P to make ATP), hyponatremia, hypernatremia
illicit drugs - immobilization with muscle tissue hypo perfusion and hypoxia, psychomotor agitation, direct myotoxicity
medications - statins, fibric acid derivatives
infections: sepsis induced hypoxia etc - Legionella most common bacterial cause
metabolic myopathies - inherited disroders
CTDs: polymyositis, DM, Sjogrens
rheum: SLE
endocrine: hypothyroidism
bio toxins: snake bikes, africanized bees, wasps,


clinical presentation of rhabdomyolysis

altered mentation with risk factors for rhabdo (intoxication, immobility, drug ingestion, electric shock, NMS)

acute renal failure with absence of cause

localized myalgais, muscle stiffness, cramping, swelling, tenderness, tea-coloured urine/.


early complications seen in rhabdomyolysis

compartment syndrome
lyte disorders/acidosis: hyperK, hyperphosphatemia, hypocalcemia early, hypercalcemia late
hepatic dysfunction - transaminitis


late complications seen in rhabdomyolysis

myoglobin induced AKI


treatment of rhabdomyolysis

fluid resuscitation - titrate to urine output above 300cc/hr
urine alkaliniazation with bicarb - controversial - if do it titrate to urine pH above 6.5 and serumpH of 7.4-7.45 and be D/Cd if calcium levels become low
mannitol - theory to increase urinary flow and wash out nephrotoxic agents - controversial - D/C if osmolal gap above 55mOSM/kg


indications for urgent dialysis

electrolyte -hyper K > 7
ingestion - of dializable subtance
overload- fluid overload