Environmental Flashcards
(190 cards)
1
Q
Four mechanisms of heat transfer
A
Conduction: direct physical contact
Convection: heat loss to air and water vapour
Radiation: heat transfer by electromagnetic waves
Evaporation: conversion of liquid to gaseous phase
2
Q
What 3 distinct functions regulate body temperature
A
Thermosensors: located peripherally and centeally; skin and in periodic anterior hypothalamus
Central integrative area: CNS creates set point
Thermoregulatory effectors: sweating and peripheral vasodilation
3
Q
What are predisposing factors for classic heat stroke
A
Advanced age Psychiatric conditions Chronic disease Obesity Certain medications
Dehydration (vomiting, diarrhea, diuretics)
Drugs (anticholinergics), skin disease, occlusive clothing
Increased heat production: exercise, drugs (synpathpmimetics), fever, delirium, thyroid storm, MH, NMS, seizures
Cardiac disease, BB drugs
Hypothalamic hemorrhage
Atherosclerosis, diabetes
4
Q
What percentage body weight loss represents moderately severe deficit
A
5-6%
5
Q
What percentage body weight loss represents severe water depletion
A
7% or more
6
Q
What is prickly heat
A
Acute inflammatory disorder of skin that occurs in tropical climates due to blockage of sweat gland pores by macerated stratum Cornell and secondary staphylococcal infection - aka miliaria, lichen tropicus, heat rash
7
Q
Clinical presentation of prickly heat
A
Prurituc vesicles on erythematous base confined to clothed areas, area often anhidrotic
8
Q
Ddx of prickly heat
A
Contact dermatitis
Cellulitis
Allergic reaction
9
Q
Treatment of prickly heat
A
Chlorhexidine in a light cream or lotion
Salicylic 1% acid can be applied to localized areas to assist in discrimination but not use in children or large areas due to risk of salicylate intoxication
Aretha Myson can use for diffuse for posture the rest of us
10
Q
What are heat cramps
A
Brief intermittent and often severe muscle cramps occurring and muscles fatigue by heavy work
11
Q
Risk factors for heat cramps
A
He cramps typically caused by salt deficiency in person to produce large amount of thermal sweat and drink copious amounts of hypertonic fluid
Often occur after exercise and while relaxing
Occupations often affected our athletes roofers steel workers coal miners field workers and boil operators
12
Q
Ddx for heat cramps
A
Hyperventilation tetany can be distinguished by the presence of carpopedal spasm’s and paraesthesias in the distal extremities and Perioral areas
13
Q
Essentials of diagnosis of heat cramps
A
Cramps of most worked muscles Usually occur after exertion Heavy sweating during exertion Copiius hypertonic fluid replacement Hyperventilation not present and cool environment
14
Q
Investigations for heat cramps
A
Lytes
They often have hyponatremia, hypochloremia
15
Q
Treatment of heat cramps
A
Mild cases without dehydration treated or early with 0.1% or 0.2% salt solution or one quarter to one half teaspoon of salt all dissolved in 1 quart of water
Severe cases respond rapidly to IV NS
16
Q
What is heat edema
A
Hydrostatic pressure and vasodilation of cutaneous vessels in heat resulting in accumulation of interstitial fluid in Lower extremities
17
Q
Ddx of heat edema
A
CHF, liver disease states,lower extremity infections, DVT
18
Q
What is heat syncope
A
Loss of consciousness and presence of heat exposure due to cutaneous vasodilation
19
Q
What are the two types of heat exhaustion
A
Water depletion heat exhaustion and salt depletion heat exhaustion
Water caused by too little replacement
Salt caused by replacement of hypotonic fluid
20
Q
Diagnosis of heat exhaustion
A
Symptoms of vague malaise fatigue and headache
Core temperature often normal and if elevated is under 40°C
Mental function essentially intact no coma or seizures
Tachycardia orthostatic hypotension and clinical dehydration may occur
Other major illness ruled out
If in doubt treat as heat stroke
21
Q
Investigations in patient with heat exhaustion
A
Electrolytes: hyponatremia, hypochloremia, and the low urinary sodium and chloride concentrations
CPK in renal function, hepatic transaminases
22
Q
Management of heat exhaustion
A
Rest
Cool environment
Assessment of volume status
Fluid replacement: normal Celine to replete volume if patient is orthostatic, replace slowly to avoid cerebral edema
Healthy young patients are treated as Outpatients
Consider admission efficient is older, has significant electrolyte abnormalities or would be at risk for recurrence if discharged
23
Q
What is the difference between heat exhaustion and heatstroke
A
Homeostatic thermoregulatory mechanisms remain intact in heat exhaustion
Heat stroke is when mechanism fails
24
Q
diagnosis of heat stroke
A
Exposure to heat stress, endogenous or exogenous
Signs of severe CNS disfunction (coma seizures delirium)
Core temperature usually above 40.5 Celsius but maybe lower
Hot skin calming and sweating may persist
Marked elevation of hepatic transaminase levels
25
What are the two forms of heat stroke
Classic and exertional
26
Characteristics of exertional heat stroke
```
Younger healthy individuals
Exercise
Sporadic
Diaphoresis
Hypoglycaemia
DIC
Rhabdomyolysis
Acute renal failure
Marked lactic acidosis
hypocalcaemia
```
27
Features of classic heat stroke
```
Older individuals with predisposing factors or medications
Sedentary
Heat wave occurrence
Anhidrosis
Normoglycemia
Mild coagulopathy
Mild to CK elevation
Oliguria
Mild acidosis
Normal calcium
```
28
Ddx of heatstroke
```
CNS hemorrhage
Toxins, drugs - anticholinergic poisoning, sympathomimetics
Seizures
Malignant hyperthermia
Neuroleptic malignant syndrome
Serotonin syndrome
Thyroid storm
High fever, sepsis
Encephalitis, meningitis
Typhoid fevers
Delirium tremens
Hypothalamic hemorrhage
```
29
Investigations for patient with heat stroke
ABG, CBC, lytes- extended, glucose, urea/Cr, CK, myoglobin and UA, transaminases, PTT, INR, lactate, troponin
30
How to cool patients with heat stroke
Preferred method : evaporative with large fans and skin wetting ; ice water immersion
```
Adjuncts
Ice packs to axilla and groin
Cooling blanket
Peritoneal lavage
Recital lavage
Gastric lavage
Cardiopulmonary bypass
```
31
Resuscitation of a patient with heat stroke
Airway control - seizures and aspiration common
Crystalloid fluid resus
Tachyarrhythnias usually resolve with cooling - avoid cardio version until myocardium cooled, avoid used of alpha adreneriv agents becuase they promote vasoconstriction and decrease cutaneous heat exchange and may exacerbate renal and hepatic damage
Atropine and antichokinfeics that inhibit sweating should be avoided
If rhabdo keep urine output at least 2ml/kg/he
Urinary alkalinization considered in patients with acids is, dehydration, or underlying renal diseS
Can give mannitol after volume to increase intravasuckar volume and gfr but don't use if oliguria
Benzos for shivering
32
What percentage of dogbite get infected and which sites are at higher risk
2 to 30%
Hand bites are at higher risk for infection
Face and scalp or a lower risk for infection
Puncture wounds at higher risk for infection than avulsions and lacerations
33
What types of bacteria are typically involved in dogbite wound infection
Often polynicrobial
Pasteurella
Other aerobics: strep, staph, Neisseria, Corynebacterium, Moraxella
Anaerobic: Fusobacterium, Bacteroides, Porphyromonas, Prevotella, and Propionibacterium
Capnocytophaga canimorsus
34
3 days typically (can be 1-10 after bite) pt develops fever, V/D, abdo pain, headache, confusion with purpuric lesions
Can also progress to endocarditis, meningitis
Capnocytophaga canimorsus
35
What patients typically affected by capnocytophaga canimorsus
Middle aged men
| Underlying medical problems most often alcoholism, splenectomy, or immunosuppression
36
What factors are high risk for bite wound infection
Species: cat, human, monkey, pig, camel, bear
Location: hand, foot
Wound type: puncture, crush injury, presence of divitalized tissue, delayed presentation (6 hours later), closed primarily
Patient characteristics: age over 50, diabetes, renal failure, liver dz, alcoholism, immune disorder, malnutrition, use of steroids or immunosuppressants, peripheral vascular disease, chronic edema of bitten area
37
What antibiotics to use for dog bite and next lines if pen allergic
Amoxicillin-clavulanate
Clindamycin + septra or cipro
Moxifloxacin
38
Antibiotics for dog and cat bites requiring hospital admission
Ampicillin/sulbactam
Piptazo
Ticarcillin/clavulanate
Clindamycin + cipro or septra
39
Indications for admission after animal bite
Structural
- injury to deep structures (bones, joints, tendons, arteries, nerves)
- injury requiring reconstructive surgery
- injuries requiring GA for appropriate wound care
Infectious
- rapidly spreading cellulitis
- significant lymphangitis or lymphadenitis
- infection of patients at high risk for complications
- infection with failed outpatient therapy
40
Antibiotic prophylaxis for human and monkey bites
Amoxclav
Moxifloxacin
Cefoxitin
Clindamycin plus penicillin or cipro
41
Antibiotics for human and monkey bite if requires admission
```
Amp/sulbactam
Piptazo
Ticarcillin/clav
Imipenem
Meropenem
Ertapenem
Clindamycin plus pen or cipro
```
42
Antibiotic prophylaxis and inpatient treatment of rodent bites
Not recommended
43
Treatment of ferret, pig, horse, bear, big cats, coyotes, wolves bites
Same as dog / cat
44
Abx prophylaxis after camel bite and treatment if admitted
Ciprofloxacin
Ofloxacin
And inpatient to same as cats and dogs
45
Rate of dog bite infection
2-30%
46
Rate of cat bite infection
80%
47
What is the major concern for exposure in monkey bites and what is it
B virus which is similar to HSV and causes vesicular lesions at site of exposure with flu like symptoms incubation period 2 days to 5 weeks
Can develop paresthesiS and muscle weakness
CNS involvement can occur which include AMS, CN palsies, ataxia, coma, respiratory failure
If left untreated mortality rate is 80%
48
Management of monkey bites
Area scrubbed with soap, or iodine, chlorhexidine then irrigated with running water for 15-20 mins
Prophylaxis with valacyclovir after high risk bites can be offered up to 5 days after bite but should be started ASAP
49
Treatment of suspected B virus infection
IV acyclovir or ganciclovir
50
When is prophylaxis for monkey B virus recommended
Skin exposure (with loss of skin integrity) or mucosal exposure to a high risk source (macaque that is ill, immunocompromised, known to be shedding virus or lesions compatible with B virus)
Inadequately cleaned skin exposure or mucosal exposure to any macaque
Deep puncture bite
Laceration of head, neck, torso
Needle stick associated with tissue or fluid from the nervous system, eyelids, mucosa, or lesions suspicious for B virus
Puncture or lacerations after exposure to objects contaminated with either fluid from monkey oral, genital, or nervous system tissues or any object known to be contaminated with B virus
A post wound cleaning culture is positive for B virus
51
What other situations can prophylaxis be considered for monkey virus B exposure
Mucosal splash that has been adequately cleaned
Laceration that was been adequately cleaned
Puncture or lac occurring after exposure to either objects contaminated with body fluid or potentially infected cell culture
52
Dosing for monkey virus B prophylaxis
Valacyclovir 1g TID for 14 days
Or acyclovir 800ng five times a day for 14 days
53
When is monkey virus B prophylaxis not recommended
Skin exposure when skin remains in tact
Exposure associated with non macaque species of non human primates
54
What is rat bite fever
Caused by Streptobacillus moniliformis or Spirillum minus
Can occur by bite, scratch or simply handling a rat
Incubation 3 days to 3 weeks
Fever, migratory polyarthralgias, maculopapular, petechial, or purpurin rash
Untreated has 10% mortality
55
Treatment of rat bite fever
IV penicillin
Streptomycin and tetracycline in penallergic patients
56
Rates of infection after clenched fist injury (fight bite)
Osteomyelitis- 16%
Septic arthritis- 12%
Tenosynovitis - 22%
57
Management of bites to oral mucosa or through and through injury
Prophylaxis of penicillin for lacs requiring primary closure and those that result in mucocutaneous communication
58
Bacteria found in human bites
Eikenella corrodens
Staph, strep, corynebacterium, fusobacterium
59
Work up of fight bite
Hand X-ray to look for retained teeth, deep structure injuries
60
When can you suture dog bites
Most except hands and feet
61
When to suture cat bite
Face only
62
When can you suture human bite or monkey
Fave only (up to 24 h after bite)
63
When to suture rodent bite
Any but rarely needed
64
When to suture ferret, pig, horse, camel, bear, big cats
Face only
65
Management of fight bite
Wound exploration through entire ROM, including closed fist when fingers are flexed, because extensor tendons and cartilage damage may not be evident in other positions
If joint, tendon or bone injury should be admitted for open debridenent and irrigation in OR - same if they present later with infected wound
think about post exposure prophylaxis if either party is known HIV positive or at high risk and blood exposure occurred, prophylaxis also indicated if HBV positive or high risk or blood/saliva exposure has occurred
66
Indications for admission for human bites to the hand
Infection at time of Presbyterian
Deep structure violations
Wound requiring OR
Patients at high risk for wound infection
Patients with likely social support or compliance issues
67
components of a focused Dive history
onset of symptoms?
type of equipment used - compressed air, mixed gas, enriched air, rebreather ? - what was source of gas
did dive approach or exceed decompression limits
was a dive computer used?
what were the number, depth, bottom time, total time and surface intervals for all dives in the 72 hours preceding symptoms
were decompression stops used? was in-water decompression attempted?
what was the time delay from last dive to air travel?
did diver experience difficulty with ear or sinus equilibration ? did pain occur n descent or ascent
was diver intoxicated, dehydrated, or working strenuously
how long after dive did symptoms start, were they present at surfacing, delayed? progressive?
is med hx of ear or sinus infections or abnormalities present? emphysema or asthma ? CAD? PFO ? neuro illness?
68
disorders that occur during descent when diving
```
middle ear barotrauma
external ear barotrauma
inner ear barotrauma
barosinusitis
facial barotrauma
```
69
disorders that arise at depth when diving
nitrogen narcosis
oxygen toxicity
contaminated air
70
disorders that arise during ascent when diving
```
alternobaric vertigo
barodontalgia
GI barotrauma
pulmonary barotrauma
decompressino sickness
arterial gas emoblism
pulmonary edema
```
71
What happens in middle ear barotrauma when diving
During descent - unsuccessful equalization causes pressure on tm,
Can cause tm rupture leading to cold water entering middle ear and causing caloric stimulation with transient nystagmus and vertigo - can also lead to 7th nerve palsy
72
What happens in external ear barotrauma when descent diving
When external auditory canal is obstructed by wax, stenosis, etc it can trap air and cause negative pressure leading to pain and or hemorrhage of the EAC
73
What happens in inner ear barotrauma upon descent when diving
Large negative pressure builds and inward deflection of tm transmits to oval window of cochlea which causes a pressure wave in perilymph which distended round window - sudden equlibratipn or valsalva and lead to hemorrhage in inner ear or tear the labyrinthine (reissner's) membrane
Symptoms are hearing loss, vertigo, nausea, tinnitus and fullness in affected ear
Signs bare nystagmus positional vertigo ataxia and vomiting
Can be challenging to distinguish from inner ear DCS
74
What is barosinusitis which occurs on descent in diving
Obstruction of sinus Ostia causes sinus barotrauma
| Most often maxillary or frontal sinus and causes facial pain and epistaxis
75
What happens with facial barotrauma with descent from diving
Pressure within dive mask over eyes and nose - if don't equalize can cause facial and conjunctival edema, petechial hemorrhages on face and subconjunctival hemorrhage
76
What is nitrogen narcosis
Intoxicating effects of increased tissue nitrogen concentration at depth
Euphoria, false feeling of well being, confusion, loss of judgement or skill disorientation inappropriate laughter diminished motor control and tingling in the vague treatment numbness of the lips and gums and legs
Occurs typically at deptus below 150 feet
77
What happens with oxygen toxicity during descent in diving
Pulmonary oxygen toxicity can present with burning sensation or pain on inspiration and coughing ; pneumonitis and permanent fibrosis are possible
CNS toxicity also occurs
78
What are possible air contaminants in scuba
CO and CO2 can contaminate compressed air tank
| Rebreathera have Ca(OH)2 which if inhaled the particles form a caustic liquid
79
What happens in alternobaric vertigo
On ascent, passive equalization of middle ear doesn't occur properly because of mucosal edema or thickening within the Eustachian tube
Pt gets vertigo, N/V
80
What is barodontalgia
Air gets trapped beneath poorly filled dental cavity or abscess and expands on ascent leading to dental pain
81
What occurs in GI barotrauma
On ascent , bowel gas expands
Predisposing factors: carbonated beverages, large meals or gas producing foods, valsalva in head down position
Symptoms- eructation, flatulence, bloating, cramps abdominal pain, can get trapped in hernia and gastric rupture possible
82
What occurs in pulmonary barotrauma
Gas bubbles forced across alveolar capillary membrane
Can cause pneumothorax , pneumomediastinum, subq emphysema, and alveolar hemorrhage
Suggestive dive features: fast ascent, panic, problems regulating buoyancy, or running out of air; pts with lung disease at risk
83
Factors that increase barotrauma in asthmatics
Bronchospasm and mucus plugging predispose local regions of lung to injury
When air is compressed it becomes denser, more turbulent flow in narrow airways
Reduction in breathing capacity with immersion
Air from compressor is cooled and may trigger bronchospasm in asthma
Exercise component of diving can trigger asthma
Compressed air may be contaminated by pollen and other allergens
84
Diving recommendations for asthma patients
Thorough h/p by physician
Asthma well controlled
Normal spirometry: FEV1 above 80%, FEV1/FVC > 75%
Succeafufl completionbof bronchial provocation challenge
Cold, exercise or emotion induced asthmatics shouldn't dive
Asthmatics requiring rescue med within 48 hours should not dive
85
What is decompression sickness
Spectrum of clinical illnesses resulting from formation of small bubbles of nitrogen gas in the blood and and tissues ascent
86
What are risk factors for decompression sickness
```
Increased length and depth of dive
Age
Obesity
Fatigue
Heavy exertion
Dehydration
Fever
Cold ambient temperatures after diving
Diving at high altitude
Flying after diving
Tobacco and alcohol use
PFO
```
87
What is difference between DCS type I and II
1 involves MSK, skin and lymphatic vessels
2 involves any other organ system
88
What is arterial gas embolism
When air bubbles escape pulmonary venous circulation and proceed to LA and LV into arterial circulation
Most common presentation is altered consciousness, dizziness, convulsions, visual changes
Can affect cerebral or cardiac circ
89
Dive history features to differentiate between DCS and AGE
DCS: depth and length dependent, decimpression limits approached , flying after diving, diving at altitude
AGE: independent of dive profile, rapid ascent, inexperience, out of air
90
Risk factors to differentiate DCS and AGE
DCS: fatigue, dehydration, fever, hypothermia, obesity, strenuous activity
AGE: obstructive lung disease, emphysema, mucus plugging, PFO
91
Symptoms and signs differentiating DCS and AGE
DCS: progressive onset, spinal symptoms predominate, ha, limb weakness or paralysis, paresthesias, abdo pain, urinary retention, fecal incontinence, periarticular joint pain, skin marbling,vertigo or nystagmus
AGE: rapid onset, cerebral symptoms predominate, ha, LOC, confusion, convulsions, motor or sensory loss, cardiac dysthymias or arrest
92
Why does DCS affect spinal Cord more than CNS
Nitrogen lipophilic and increased concentration of lipids in spinal cord
93
Extra physical exam maneuver to help with DCS I if complaining of joint pain
Put bp cuff over joint and inflate to 150-200 - pt may experience relief if due to bubble in joint
94
Management of patients with suspected dive injuries
100% O2 until pulmonary barotrauma or DCS ruled out if vitals stable
ACLS if unstable
Call DAN
Rehydration if suspected nonpulmonary DCS (chokes)
Recompression when indicated
95
Diving disorders that require recompression therapy
DCS I and II
AGE
Contaminated air (CO poisoning)
96
Management of external ear barotrauma, middle ear barotrauma and internal ear barotrauma
External ear- clean external canal and remove foreign bodies
Middle ear - topical nasal vasoconstrictors like phenylephroje and oxymetalozine and repeated maneuvers to displace fluid through the eustschian tube
If ruptured tm, prophylactic oral abx
Oral steroid if CN7 palsy
IEBT- bed rest for 5-7 days with head elevated, avoid straining, decongestants to facilitate draining of middle ear, refer to otolaryngology
97
define drowning
the process of experiencing respiratory impairment from submersion/immersion in liquid
98
define immersion syndrome
syncope resulting from cardiac dysrhythmias on sudden contact with water that is at least 5C lower than body temperature
proposed cause: vagal stimulation leading to systole and VF secondary to QT prolongation after massive release of catecholamines on contact with cold water
99
risk factors for drowning
age: toddlers and those over 75
boys account for 80% of victims older than 1 year old
aboriginal for all age groups
black 11-12 year olds drown 10x more often than white kids
EtOH consumption
time of year- May-August in US
more likely on weekends
medical conditions: seizure disorders, autism and other developmental/behavioural disorders
cold water - increased dysrhythmia in those with long QT
100
pathophysiology of drowning
submersion -> breath holding, panic --> air hunger and hypoxia develop --> victim swallows water
aspiration of -2ml/kg of fresh or salt water destroys pulmonary surfactant leading to alveolar collapse, atelectasis, noncardiogenic pulmonary deem, intrapulmonary shunting and VQ mismatch
profound hypoxia and metabolic and respiratory acidoses ensure, leading to CV collapse, neuronal injury and death
101
factors influencing the pathophysiology of drowning which may affect survival
age: children lower ratio of body mass to surface area and therefore develop hypothermia more quickly and to a greater degree
water temp: cold water speeds the development of exhaustion, altered consciousness, and cardiac dysrhythmias
duration and degree of hypothermia: hypothermia lowers cerebral metabolic rate and is neuroprotective; however hypothermia usually poor prognostic factor
diving reflex: infants/children- immersion of face in cold water shunts blood centrally to heart and brain - apnea and bradycardia ensue, prolonging the duration of submersion tolerated without CNS damage
effectiveness of resuscitation efforts
102
prognostic factors in drowning
hypoxia which is dependent on submersion time is most important factor affecting outcome and QOL
poor outcome: age under 3, submersion longer than 5-10 minutes, and initiation of CPR more than 10 mins after rescue
neuro findings on initial presentation + victims whose submersion or resus longer than 10 mins usually unfavourable outcome
objective findings with poor prognosis: hypothermia, severe acidosis, unreactive pupils, GCS 3, asystole, or need for ongoing CPR
children with abnormal head CT (ICH, cerebral deem) within first 24 hours have nearly 100% mortality rate
abnormal CT at any time correlated with poor outcome (death or persistent vegetative state)
103
DDX/considerations in drowning
precipitants of drowning: EtOH, cardiac arrest, hypoglycaemia, seizure, attempted suicide or homicide
peds: child abuse or neglect
potential head or C spine injury
104
work up of drowning
cardiac monitoring and ECG to look for dysrhythmias , QT prolongation or ischemia
pulse ox, capnography, and ABG to look for hypoxemia, hypercarbia, and acidosis
glucose, Cr, lytes
CBC
EtOH, urine tox
subsequently, evidence of renal failure, hepatic dysfunction and DIC may be noted (N on initial labs)
CXR - repeat as infiltrates and deem may be evident within hours
EEG to assess for seizure activity in obtunded drowning victims
CT head rarely contributory initially unless significant trauma
MRI not prognostic until 3 or 4 days elapse
105
which drowning patients at risk for C spine injury and who needs a collar
ones who have clinical signs of serious trauma or hx of MVC, fall from height or diving into water - collar these ones, not needed if none of these risk factors present
106
indications for intubation of drowning patient
apparent or developing respiratory distress, absence of protective airway reflexes, significant associated head or chest injuries, PaCO2 > 50, unable to maintain sat above 90 or PaO2 < 60 on high flow, requiring PPV
107
when to use empirical abx in drowning patient
they do not increase survival so only in patient who was submerged in grossly contaminated water or who shows signs of infection or sepsis
108
management of drowning patient after resus
rewarming should not go above 34C, followed by 24 hour mild hypothermic treatment before normothremia causes decreased pulmonary reperfusion injury and reduced secondary brain injury
109
which drowning patients can be discharged from ED
asymptomatic on presentation to ED, maininta normal O2 sat on room air, no CXR or ABG abnormalities after observing them for 6 hours
110
define hypothermia
core temp below 35C
111
factors predisposing to hypothermia
```
decreased heat production:
endocrine failure
hypopituitarism
hypothyroidism
diabetes
insufficient fuel
hypoglycemia
malnutrition
marasmus
kwashiorkor
extreme exertion
neuromuscular inefficiency
age extremes
impaired shivering
inactivity
lack of adaptation
```
```
increased heat loss:
environmental
immersion
non immersion
induced vasodilation
pharmacologic
toxicologic
erythrodermas
burns
psoriasis
ichthyosis
exfoliative dermatitis
iatrogenic
emergency deliveries
cold infusions
heat stroke treatment
```
```
impaired thermoregulation:
peripheral failure
neuropathies
acute spinal cord transection
central failure, neuro
CNS trauma
toxicologic
metabolic
SAH
pharmacologic
hypothalamic dysfunction
Parkinson's disease
anorexia nervosa
cerebellar lesion
neoplasm
congenital intracranial abnoramlities
MS
```
```
miscellaneous associated clinical states:
recurrent or episode hypotehrmia
sepsis
pancreatitis
carcinomatosis
CP disease
vascular insufficiency
uremia
Paget's disease
GCA
sarcoidosis
shaken baby syndrome
multisystem trauma
Shapiro's syndrome
Wernicke-Korsakoff syndrome
Hodgkin's disease
```
112
heat conservation mechanisms by temperature range
30-37C - vasoconstriction, shivering, and non shivering basal and endocrinology thermogenesis create heat
24-30C- progressive depression of basal metabolic rate without shivering
below 24- autonomic and endocrinology mechanisms for heat conservation become inactive
113
physiologic effects of hypothermia on CV system
initial tachycardia followed by progressive bradycardia
pulse decreases by 50% at 28 C
atrial and ventricular dysrhythmias common in moderate or severe hypothermia
114
ECG findings of hypothermia
Osborn (J) wave seen at junction of QRS complex and ST segment
as hypothermia worsens PR interval, then QRS interval, then QTc become prolonged
115
DDX for J waves on ECG
```
local cardiac ischemia
sepsis
CNS lesions
hypercalcemia
BER
Brugada
```
116
what is core temp afterdrop
decrease in individual's core temp after removal from cold, temperature equilibration by conduction and countercurrent cooling of blood perfusing cold tissues results in greater decrease in core temp
117
how to prevent core temperature afterdrop
active external rewarming of extremities abolishes peripheral vasoconstriction and reverses AV shunting
118
physiologic effects of hypothermia on CNS
hypothermia depresses CNS
EEG silence at 19-20C
cerebral auto regulation maintained with an increased in vascular resistance until 25C
119
physiologic effects of hypothermia on kidneys
exposure to cold induces a diuresis
120
physiologic effects of hypothermia on respiratory system
stimulates respiration followed by progressive decrease in respiratory minute volume
CO2 production decreased by 50% with an 8C decrease in temp
CO2 retention with resp acidosis can occur
vicious bronchorrhea, decreased ciliary motility, and noncardiogenic pulmonary edema
121
clinical presentation of hypothermia by system
HEENT: mydriasis, decreased corneal reflexes, EOM abnormalities, erythopsia, flushing, facial deem, epistaxis, rhinorrhea, strabismus
CV: initial tachycardia, subsequent bradycardia, dysrhythmias , decreased heart tones, hepatojugular reflux, JVD, hypotension
resp: initial tachypnea, adventist sounds, bronchorrhea, progressive hypoventilation, apnea
GI: ileus, constipation, abdo distension or rigidity, poor rectal tone, gastric dilation in neonates or in adults with myxoedema
GU: anuria, oliguria, polyuria, testicular torsion
neuro: depressed LOC, ataxia, hypesthesia, dysarthria, antinociception, amnesia, initial hyperreflexia, areflexia, central pontine myelinolysis
psych: impaired judgment, perseveration, mood changes, peculiar flat affect, AMS, paradoxical undressing, neuroses, psychoses, suicdie, organic brain syndrome
MSK: increased muscle tone, shivering, rigidity or pseudo-rigor mortis, opisthotonos, compartment syndrome
derm: erythema, pernio, pallor, frosting, cyanosis, frostbite, icterus, popsicle panniculutis, sclera, cold urticaria, ecchymosis, necrosis, deem, gangrene
122
what reflex is last to disappear and first to reappear in hypothermia
knee jerk
123
DDX of hypothermia
hypothyroidism, hypopituitarism, diabetes, hypoglycaemia, malnutrition, intracranial and spinal cord injuries and sedative/hypnotic and EtOH intoxication
infection: GN sepsis, pneumonia, meningitis, encephaltiis, endocarditis, brucellosis, malaria, syphillis, typhoid, military tb, trypanosomiasis
carcinoma, pancreatitis, peritonitis, and cerebrovascula disease
low CO from MI can cause hypothermia
MgSO4 during labour
delayed recovery from NM blockade
124
lab workup of hypothermic patient
glucose, CBC, lytes, lipase, coags, urea/Cr, VBG
EtOH level, urine too if LOC inconsistent with degree of hypothermia
thyroid functions, cardiac markers and serum cortisol may also be indicated
125
changes in heme labs in hypothermic patient
HCT increases 2% for every 1C fall in temp, so if pt HCT is low-normal, consider blood loss
decreased WBC and platelet counts due to sequestration
hyper coagulable state - can progress to DIC, enzymatic activity of activated clotting factors is depressed by the cold
126
what to suspect if hypothermic patient remains hyperglycemic during rewarming
hemorrhagic pancreatitis or DKA
127
how to interpret ABG in hypothermic patient
blood gases analyzer warms sample to higher O2 and CO2 samples and lower pH than in vivo
target to uncorrected pH of 7.4, PaCO2 of 40
128
how to treat coagulopathy in hypothermia patient
rewarm them is ONLY treatment
| do not give clotting factors
129
management of hypothermic patient
monitor with continuous core temp - rectal 15cm or esophageal
cardiac US prior to startgin compressions
intubation as necessary, NG tube afterward
continuous cardiac monitoring
catheter for urine output
IV fluids- warm 500cc NS bolus
ACLS- CPR until warm, if pt in VF can defibrillate x 1 and then warm to above 30C and further attempts can be made, don't use epinephrine below 30
treatment of ventricular dysrhythmias - amio can increase torsades, procainamide can increase VF, but quinidine has been shown to prevent VF during induced profound hypothermia and during cardiac manipulation at 25-30C
pacing- transcutaneous pacing ; don't do transvenous because hazardous for bradydysrhythmias
abx: empirical if under 3 months, older adults as well, treat any cellulitis, myositis, bacteriuria or infiltrate on CXR in other ages
hydrocortisone 100mg IV if failure to rewarm and suspect adrenal insufficiency or steroid dependence
thyroid if pt thought to have myxoedema - or if hx hypothyroidism, neck scar or failure to rewarm
130
what is leading cause of failure to rewarm in hypothermic patietn
infection
131
what is passive external rewarming and when is it used
used in patients with mild hypothermia and active rewarming is not available
covering the patient in an insulating material in a favourable atmospheric condition, ambient temp should exceed 21C
132
what is active rewarming
direct transfer of exogenous heat to the patient - can be internal or external
133
indications for active rewarming
CV instability
moderate or severe hypothermia (<32C)
inadequate rate of rewarming or failure to rewarm
endocrinologic insufficiency (hypopituitarism, hypothyroidism, hypoadrenalism, and Wernicke's)
traumatic or toxicological peripheral vasodilation (spinal cord transection )
secondary hypothermia impairing thermoregulation (i.e.. stroke) (DKA because insulin not effective until T > 30C)
134
how to rewarm hypothermic patients
AER - ie. bair hugger - forced air warming that transfers large amount of heat and minimizes after drop
heated humidified O2 and warmed IV fluids in addition to AER may help prevent hypoxia, metabolic acidosis, core temp after drop and hypotension
AER + 1 or more active core rewarming for moderate to severe hypothermia
```
airway rewarming - heated humidified O2
peritoneal dialysis with dialyste at 40-45C
heated irrigation- thoracic lavage
endovascular rewarming
diathermy
extracorporeal blood rewarming
```
135
freezing injury cascade
prefreeze phase: superficial tissue cooling, increased viscosity of vascular contents, microvascular constriction, endothelial plasma leakage
freeze-thaw phase: ECF ice crystal fluid formation, water movement across cell membrane, intracellular dehydration an dheyperosmolality, cell membrane denaturation or disruption, cell shrinkage and collapse
vascular stasis and progressive ischemia:
136
predisposing factors for peripheral cold injury
physiologic: genetic, core temp, previous cold injury, acclimatization, dehydration, overexertion, trauma-multisystem, extremity, dermatologic disease, physical conditioning, diaphoresis, hyperhidrosis, hypoxia
mechanical: constricting or wet clothing, tight boots, vapour barrier, inadequate insulation, immobility or cramped position
psychological: mental status, fear, panic, attitude, peer pressure, fatigue, intense concentration on tasks, hunger, malnutrition, intoxicants
environmental: ambient temperature, humidity, duration of exposure, wind chill factor, altitude and associated conditions, quantity of exposed surface area, heat loss- connective, evaporative, aerosol propellants, CV, hypotension, atherosclerosis, arteritis, Raynaud's, cold-induced vasodilation, anemia, sickle cell disease, diabetes, vasoconstrictors, vasodilators
137
define frostnip
superficial freezing injury manifested by transient numbness and tingling that resolves after rewarming
no tissue destruction occurs
138
favourable initial symptoms after rewarming cold injury
normal sensnation, warmth and color
early formation of clear fluid filled blebs is more favourable and than delayed appearance of smaller, more proximal hemorrhagic vesicles that are produced by damage do to subdermal vascular plexi
139
work up of patient with frostbite
lab testing and imaging for coexisting conditions and injuries
Xray baseline of frostbite tissue - f/u in 4-10 weeks may begin to demonstrate specific frostbite abnormalities
pts being considered for lytics should undergo CTA or MRA
140
sequelae of frostbite and nonfreezing cold injuries
neuropathic: pain (phantom pain, CRPS, chronic pain), sensation (hypesthesia, dysesthesia, parenthesis, anesthesia), thermal sensitivity, autonomic dysfunction (hyperhidrosis, Raynaud's)
MSK: atrophy, compartment syndrome, rhabdomyolysis, tenosynovitis, stricture, epiphyseal fusion, OA, osteolytic lesions, subchondral cysts, necrosis, amputation
derm: edema, lymphedema, chronic or recurrent ulcers, epidermoid or squamous cell carcinoma, hair or nail deformities
misc: core temp afterdrop, ATN, electrolyte fluxes, psychological stress, gangrene, sepsis
141
prehospital mgmt of frostbite/cold injuries
remove constricting/wet clothing and insulate/immobilize affected area
massage NOT effective and increases tissue loss
frozen parts kept away from dry heat sources during transport
do not rewarm in field if any possiblign that thawing will be incomplete or that tissue will refreeze during evacuation
when evacuation not possible - rapid field rewarming in water at 37-39C
142
ED rewarming protocol of frostbite/cold injuries
prethaw: assess Doppler pulses and appearance, protect part - no friction massage, stabilize core temp, address med/surg conditions, administer volume replacement pre
thaw: provide parenteral opiate analgesia as needed, administer ibuprofen 400-600mg (or asa 325)
immerse part in water at 37-39C
encourage gentle motion but do not massage
post-thaw:
dry and elevate, aspirate or debride clear vesicles, decried and apply topic antibiotic or sterile aloe vera q6h, leave hemorrhagic vesicles in tact
tetanus prophylaxis
provide strep prophylaxis if high risk
consider phenoxybenzamine in severe cases
performing imaging including angiography if lysis may be indicated
carrot out thrombolysis if indicated and available
obtain admission photographs
143
what is pernio/chilblains
cold sores appear with 24 hours of cold exposure usually on face, dorsal on hands and feet and pretibial areas
144
treatment of pernio
v. painful may need opioids
| nifedipine 20-60mg daily used in severe pernio
145
treatment of immersion injury
rewarm slowly
local cooling lowers metabolic requirements and improves pain and deem - cooling should be continued until hyperaemia resolves
146
what is the leading cause of death from altitude illness
high altitude pulmonary edema
147
factors influencing acute mountain illness
```
elevation and rapidity of ascent
prior acclimatization
individual genetic susceptiblity
sleeping elevation
duration of stay
```
148
what heights are deemed moderate and high and very high and extreme altitude
moderate: 5000-8000 feet
high: 8000-14000 feet
very high: 14000-18000 feet
extreme: over 18000
149
why does O2 change at higher altitudes
hypobaric hypoxia
occurs because Patm decreases at elevation and therefore partial pressure of O2 decreases
150
physiologic changes with occur with acclimatization to altitude
increase in minute ventilation - carotid bodies detect hypoxia within minutes of elevation and signal response control centre in medulla to increase ventilation
respiratory alkalosis develops, kidneys begin to excrete bicarbonate - acetazolamide enhances this excretion
hypoxia leads to release of catecholamines which increases CO, HR, SV, BP and venous tone
heme: increased Hb and #RBCs
increased 2,3-DPG, shifting O2-Hb dissociation curve, favouring release of O2 from blood to tissues; leftward shift caused by respiratory alkalosis counteracts this
151
timing of typical development of HACE and HAPE
2-4 days after exposure to high altitiude
152
Lake Louise criteria for the diagnosis of acute mountain illness
pt to have recently ascended to an elevation of 8000 feet, with headache PLUS one of: GI upset (anorexia, N/V), general weakness or fatigue, dizziness or lightheadedness, or difficulty in sleeping
h/a typically worse during night and on awaking or on suddenly becoming upright
timing: few hours after arrival at altitude and reaches max severity between 24-48 hours
153
DDX for acute mountain sickness
```
tension headache
viral prodrome
EtOH intoxication/toxidrome
CO poisoning
dehydration
caffeine withdrawal
migraine h/a
infectious (mengintis, encephalitis/ viral syndrome)
intracranial hemorrhage or mass
CNS aneurysm
venous sinus thrombosis
abdominal process (ie. gastro)
AACG/ocular process
```
154
treatment of acute mountain sickness
should not ascend to higher sleeping altitude until symptoms resolve to allow acclimatization to occur (may take 1-4 days)
if pt develops neuro abnormalities or evidence of severe pulmonary deem - immediate descent indicated
supplemental O2 - lifesaving in severe
h/a - tx with asa, ibuprofen, acetaminophen
N/V- prochlorperazine cause stimulates HVR (hypoxic ventilatory response)
acetazolamide - prevents periodic breathing and eradicates insomnia; accelerates acclimatization
dexamethasone - only use when rapid ascent needed or in people with acetazolamide intolerance, does not improve acclimatization
155
prevention of acute mountain sickness
gradual ascent to allow acclimatizaiton
high carb diet
avoidance of EtOH or smoking
acetazolmaide if ascent is rapid or known history of recurrent acute mountain sickness - 250mg BID 24 hours before ascent and continuing for first 2 days at high altitude is effective
156
Clinical presentation of HAPE
Dyspnea at rest, cough, anorexia, cyanosis, rales, tachypnea, tachycardia
Usually 2-4 days after arrival at high altitude
157
Treatment of HAPE
Mild - may recover with bed rest
Moderate- bed rest and supplemental O2
Severe - O2 and descent, hyperbaric if available; if O2 and descent not possible then nifedipine 30mg SR q12h, consider acetazolamide 125-250 and tadalafil 10mg q12h
158
DDx of HAPE
```
CO poisoning
Pneumonia
Pneumothorax
Pleural effusion
PE
ACS
CHF
AE of preexisting PH
AECOPD
Acute asthma flare
Acute exacerbation of valvular disease (insufficiency and stenosis)
```
159
Ultrasound findings in HAPE
Lung comet tails - B lines indicate extravascular water
Demonstration of high pulmonary artery pressure with normal LV function
160
CXR findings in HAPE
Unilateral infiltrates may be seen in mild cases, bilateral in more advanced
Involvement of RML most common
Pleural effusion may be present in severe cases
161
ECG findings in HAPE
Tachycardia
Evidence of R sided heart strain
Right axis deviation, P wave abnormalities, tall R waves in precordial leads, S wave in lateral leads
162
Hemodynamic findings in HAPE
Increased pulmonary vascular resistance
Elevated PA pressures
Normal pulmonary wedge pressures
163
How does nifedipine help in HAPE
Lowers PA pressure, pulmonary blood volume, and pulmonary vascular resistance or enhance alveolar fluid clearance
164
Clinical presentation of HACE
Ataxia, severe headache, N/V, altered mentation, seizures, coma
Although severe symptoms usually develop within 1-3 days, may not occur until 5-9 days
165
Ddx of HACE
```
Acute CVA
ICH
Hypoglycaemia
CO poisoning
Meningitis/encephalitis
Hypothermia
Intracranial mass
Vertebral/ carotid dissection or stenosis
Acute toxidrome - EtOH or other
Acute EtOH withdrawal/ DTs
Seizure
Transient global amnesia
```
166
Treatment of HACE
Immediate evacuation to lower altitude, O2, bedrest, dexamethasone 8mg IV or Po then 4mg q6h, hyperbaric therapy if unable to immediately descend
167
Medical conditions that make travel to altitude contraindicated
Sickle cell anemia
Severe COPD
Symptomatic PH
Uncompensated CHF
168
Medical conditions that require caution when traveling to altitude
```
Moderate COPD
Asymptomstic PH
Compensated CHF
Morbid obesity
Sleep apnea syndromes
Troublesome arrhythmia
Stable angina or CAD
High risk pregnancy
Sickle cell trait
Cerebrovascular diseases
Any cause of restricted pulmonary circulation
Seizure disorder (not on meds)
Radial keratotomy
```
169
what are the 3 main epidemiological groups who get electrical injuries
toddlaers/younger children: low voltage injuries in household as a result of contac t wit electric sockets and cords
adolescents and young adults: high voltage injury y from contact with electic lines outside of houes
men in 3rd/4th decade due to occupational injuries to due to high voltage encounters
170
factors affecting electrical injury
```
circuit type: AC more dangerous than DC
amperage
resistance: different tissues have different resistance
voltage
current pathway
current duration
```
171
physical effects of different amperage levels
1mA- barely perceptible
6-9mA- usually range of let-go current
16mA- max current that an average person can grasp and let go
20mA- paralysis of respiratory muscles
100mA- VF threshold
2A- cardiac standstill and internal organ damage
172
electrical formulae- Joule's law
P= I^2RT
I=V/R
173
resistance of body tissues from lowest to highest
```
nerve
blood vessels
muscle
skin
tendon
fat
bone
```
174
tips to avoid lightnin strike
seek shelter inside an enclosed building or metal-toped car
avoid large flat, open areas or hilltops
avoid contact with metal objects and remove metal objects such as jewelry or hairpins
avoid trees, boats and open water
if caught on open ground, curl up on your side with hands and feet close together to reduce contact points or squat with feet together; if possible place rubber raincoat under your body ro feet to reduce ground current effects
if in a forest, seek shelter under a thick growth of short trees
if indoors, avoid use of wired phones and contact with plumbing or electrical appliances
175
types of burns associated with electrical injury
entrance/exit site burns
arc burns
thermal burns
flash burns
176
ECG changes seen with lightning strike
```
ST segment elevation
QT interval prolongation
atrial fib
inverted or flattened T waves
MI pattern without cardiac sequelae
```
177
effects on CV system following electrical injury
sinus tachy or brady, a fib, ectopic beats, VF, asystole
transient ST segment elevation or depression that does not correlate with myocardial ischemia
resp arrest can occur as a result of tetanic paralysis of thoracic respiratory muscles
178
effects on head/neck in electrical injuries
```
ocular involvement -cataracts most common
vitreous/anterior chamber hemorrhages
retinal detachment
macular lacerations
corneal/conjuntival burns
sensorineural deafness
vertigo
orofacial injuries in toddlers that eat cords - complication of delayed labial artery bleeding can occur 2 days after injury
```
179
extremity injuries caused by electrical injury
muscle necrosis
vascular injury - intima - immediate coagulative necrosis and thrombosis; media- aneurysmal dilation and hemorrhage in a delayed fashion
risk of compartment syndrome
bone injury- periosteal burns and osteonecrosis
DC current causes strong muscle contraction throwing victim away from source can cause fracture/dislocations; AC causes muscular tetany which can cause similar skeletal
180
nervous system effects of electrical injuries
CNS: altered mental status, seizure, coma
transient spastic paralysis, delayed/chornic: ascending paralysis, transverse myelitis, ALS
peripheral neuropathies
neuropsych: anxiety, depression, mood lability, difficulty concentrating, insomnia
181
CV effects of lightning injury
cardiac/resp arrest
asystole
myocardial contusion (most common)
MI
182
what are Lichtenberg figures
superficial fernlike burns that occur in lightning strike burns
183
what is keraunoparalysis
lightning strike victim wakes up to find themselves on the ground unable to move limbs
184
effect of lightning strike on ears
TM commonly ruptured
bleeding and CSF leaks may accompany this injury
other effects: avulsion of mastoid process, ossicle damage, rupture of Meissner's membrane, strial degeneration
symptoms: hearing loss, tinnitus, vertigo and nystagmus
185
findings suggestive of a lightning strike
clothing wet from rain
tears or disintegration of clothing
multiple victims
typical arborescent pattern of erythema or superficial linear or punctate burns
tympanic membrane injury
cataracts, especially in a younger patient
magnetization of metallic objects on body or clothing
ECG changes
186
which electrically injured patients need further investigations
those exposed to high voltage sound
any voltage with: LOC, altered mental status or neuro deficits, significant symptoms, entrance and exit wounds and/or burns assessed as being more than superficial partial thickness burns
187
work up required for electrical injury patients
ECG
CBC, lytes, Cr/urea, troponin, myoglobin, UA for myoglobin
if suspected intraabdominal injury: hepatic/pancreatic enzyme levels, coags
Xray of injured extremities
CT/MRI indicated when intracranial, spinal, intra-abdominal or pelvic injuries clinically suspected
188
workup of patient with lightning injury
ECG of strike victims with high risk indicators: suspected direct strike, LOC, focal neuro complaint, chest pain or SOB, associated traumatic injuries, pregnancy and burns of the cranium or legs or on more than 10%
complaints of diffuse muscle pain or findings of compartment syndrome - evaluation for rhabdo and vascular insufficiency bearing in mind lightning has unique effects on vascular system that often clear without sequelae
cardiac markers often elevated but don't correlate with myocardial injury and are not prognostic
189
management of electrical injury patients
arrest - resus regardless of rhythm -good outcomes seen with asystole
fluid mgmt similar to crush injuries - IV crystalloids titrated to maintain urine output over 100mL/r in adults and 1.5-2ml/kg/hr in young children
monitor serum K in patients with renal insufficiency or myoglobinuria
if hypotensive- look for possible blood loss from traumatic injuries
who needs extra monitoring: ECG signs of cardiac inury/dysrhymia, more than minimal local signs and symptoms; peds pt with oral injuries hospitalize for hydration, wound and pain mgmt, plastic surg consult; pregnant patients should receive period of fetal monitoring
can pull out taser barbs with firm in line traction
190
management of lightning injury patients
can get extensive catecholamine release or autonomic stimulation - transient hypertension and tachycardia can be treated with BB, hydrazine or with alpha blockers
DC curent - transient vasospasm that results in blue, mottled, pulseless extremities - think about this when planning surgical intervention - may be TRANSIENT only
central line to assess volume status correctly as pulses extremities may limit ability to detect hypotension
can get fixed pupils, etc in absence of irreversible brain injury, so don't use this to prognosticate in resuscitations
disposition: direct lightning strike or abnormal ECG - telemetry monitoring for minimum 24 hours
D/C instructions: seek care if develop delayed onset symptoms - CP, neuro, psych, optho or ENT in nature
