Chp. 26 Hyperthermia Flashcards

1
Q

How do patients become hyperthermic under ax?

A
  • Body temp usually balanced btw metabolic generation of heat and processes of heat loss
  • Patient warming during ax, sx almost always necessary to avoid hypothermia
  • Accidental hyperthermia most often cause
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2
Q

Causes of accidental hyperthermia

A
  • Warm ambient temperatures
  • Larger animals with thick air coats
  • Use of active external warming devices
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3
Q

What is the most common contributory cause of Perioperative hyperthermia?

A
  • excessive external heating
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4
Q

T/F: increased body temp is far less common in the context of anesthesia, surgery than decreased body temp, particularly in small patients

A

True

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5
Q

Body temp may rise to above normal levels by three mechanisms:

A

1) Decreased loss of body heat through increased insulation, particularly in larger patients with extensive insulating hair coats plus added insulation or padding
2) Excessive or poorly controlled exogenous heating, often in combination with increased insulation or other environmental factors
3) Increased metabolic production of heat including stress-related hyperthermia, increased muscle tone, resetting of thermoregulatory processes and rarely MH or related syndromes

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6
Q

What are the four main mechanisms of heat loss?

A

1) Radiation
2) Convection
3) Conduction
4) Evaporation of moisture from skin and respiratory tract
(5) excretion of urine and feces)

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7
Q

What are the two most significant sources of heat loss?

A
  • Radiation
  • Evaporation –> considerable species variability in strategies for evaporative heat loss eg panting in dogs, sweating in horses, humans
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8
Q

In a normal awake subjects…

A
  • Relative contribution of each mechanism varies also with ambient temperature, humidity, windspeed
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9
Q

At high ambient temperatures, severe and sustained exercise…

A

…Can generate heat through metabolic work in excess of capacity of heat loss mechanisms

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10
Q

Fever vs Hyperthermia?

A
  • Fever: regulated increase in core body temp
  • Hyperthermia: more general term referring to an increase in body temp, based on any etiology
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11
Q

What is significant perioperative hyperthermia in cats and dogs?

A
  • Hyperthermia of even degree or two increases circulatory work
  • More extreme increases in body temp (>42C/108F) increase metabolic rate, consume energy substrate, and increase oxygen utilization beyond oxygen supply
  • Cellular hypoxia results with potential damage to brain, livers, kidneys and blood
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12
Q

At what level is active cooling warranted?

A
  • Moderate hyperthermia with temperatures <42*C requires active cooling and dedicated monitoring of organ function
  • Specific therapy for organ damage may not be needed unless patients otherwise compromised
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13
Q

How should moderate hyperthermia be managed?

A
  • Identification of underlying cause/causes (usually excessive external heating) and corrected
  • Supplemental oxygen: avoid rebreathing, CO2 retention
  • Increases in convective and conductive heat loss often suffice to reduce body temperature
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14
Q

How to increase evaporative cooling?

A
  • Application of alcohol or water to the skin and by use of a fan to increase airflow across the skin
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15
Q

How to increase conductive heat loss?

A
  • Contact with cold packs, with caution to avoid tissue damage
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16
Q

Administration of cool IV fluids -

A
  • Increases cooling
  • Increases peripheral perfusion
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17
Q

More aggressive methods of cooling include?

A
  • Cool or cold water immersion
  • Cool enemas
  • Gastric or abdominal lavage
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18
Q

What is important to remember about active cooling?

A
  • Important to discontinue active cooling before return of body temperature to normal DT “after drop”
19
Q

“Afterdrop”

A

Continued decrease in body temperature after removal of cooling methods
–Difficult to anticipate extent of continued decrease in body temperature

20
Q

When should cooling be discontinued?

A

Once body temp decreases below 40C/104F

21
Q

What additional steps should be taken when hyperthermia is more severe, with body temp above ~42*?

A
  • Continued monitoring of body temp
  • Repeated evaluation of multiple organ systems for signs of compromise or failure
  • Eval for: acidosis, renal and hepatic fxn, evidence of DIC or other coagulopathy, neurologic fxn, cardiac fxn
22
Q

Should antipyretics be used in treating hyperthermia?

A
  • Dipyrone or other antipyretics may lower hypothalamic thermostatic control of body temperature but rarely, if ever, indicated for control of hyperthermia
23
Q

What is malignant hyperthermia?

A
  • Rare syndrome most fully described in human patients and several strains of purebred swine
  • Susceptible individuals may develop syndrome of progressive and potentially fatal hyperthermia that is “triggered” by commonly used anesthetics
  • Suspected in other species including dogs, cats, horses
24
Q

Signs of MH

A
  • Increased body metabolism
  • Muscle rigidity
  • Eventual hyperthermia, which may exceed 110*F
  • Death can result from cardiac arrest, brain damage, internal hemorrhaging or failure of other body systems
25
Q

Classical MH

A
  • Originally described as a syndrome including progressive muscle rigidity, tachycardia, and fever
  • “Pharmacogenetic” disorder in that genetically susceptible individuals may develop the syndrome upon exposure to specific “triggering” drug
26
Q

MHAUS

A

Malignant Hyperthermia Association of the United States

Informative, useful source of support, information, and referral network dedicated to MH and related syndromes in human patients

27
Q

What is the underlying pathophysiology of MH syndrome?

A
  • Abnormal mechanism for release of calcium from SR and abnormal calcium channel function
  • Calcium excess through to represent the functional deficit in classical MH
  • Excess concentration of calcium in mycoplasma induces extraordinary catabolic aerobic and anaerobic metabolic reactions
28
Q

What is the heritability of MH in humans?

A
  • Autosomal dominant mode of inheritance
  • Rate of occurrence in humans estimated to be as frequent as 1/5000 or as rare as 1/65,000 administration of ax
29
Q

T/F: Genetic component of classical MH supported by data in humans, pigs, and most recently dogs

A

True

30
Q

How does the presentation of classical MH syndrome in dogs differ from signs described for the MH syndrome in humans and swine?

A
  • Rapid increases in temperature and increased ETCO2
31
Q

What are the classical signs of MH syndrome in humans and swine?

A

Muscle rigidity
Acidosis

32
Q

Which anesthetics are recognized as potential triggering agents for MH?

A

Classically recognized anesthetic drugs that may initiate an episode of MH in susceptible individuals:
- All volatile agents
- Succinylcholine

33
Q

T/F: MH, or closely related syndromes, may occur in apparent absence of specific triggering agents

A

True

34
Q

Are these non classic episodes mechanistically identical to MH?

A
  • Controversial
  • Non-classic episodes, like many syndromes symptomatically resembling MH, may respond differently to therapy and may also have considerably more favorable prognosis
35
Q

How is MH treated?

A

AGGRESSIVELY
- Immediate removal of possible triggering agents
- Aggressive IVF
- Tx for hypoxia
- Administration of dextrose for brain metabolism
- Active cooling
- Administration of dantrolene sodium
- Management of acidosis if present
- Other therapies as indicated by intensive monitoring or patient evaluation

36
Q

How does dantrolene sodium work in the treatment of MH?

A
  • Intracellular calcium levels become abnormally elevated -> dantrolene counteracts this abnormality by preventing ongoing release of calcium from SR storage sites in muscle
  • Through control of ca release, thought to reduce muscle tone and metabolism
37
Q

What are the SE effects of dantrolene therapy?

A

Muscle weakness

38
Q

What is a limiting feature of dantrolene in veterinary medicine?

A

Expensive

Has been used with variable success in treatment of MH and MH-like syndromes in animals

39
Q

T/F: Dantrolene is recognized as an essential and life-saving component of immediate treatment of MH in human patients

A

True

40
Q

What syndromes are related to MH?

A
  • Malignant neuroleptic syndrome documented in dogs, humans
  • Key features: underlying (presumably inherited) susceptibility and exposure to a triggering pharmaceutical, typically a major tranquilizer
  • Substantial exercise, excitement, psychological or physiologic stresses recognized as contributing factors
  • MH-like syndromes suggested as causes of mortality in exercise-induced heat stroke
  • Postoperative, post anesthetic myopathies in horses have been compared to classical MH
41
Q

What anesthetics, anesthetic techniques recommended as relatively safe for patients with medical histories suggesting a susceptibility to MH-like syndromes?

A
  • Avoidance of triggering agents, particularly inhalants and succinylcholine
  • Accepted medications: tranquilizer and opioid preanesthetics, propofol induction and infusions for maintenance of GA, fent CRU for added pain management if necessary
42
Q

What are other causes of postoperative hyperthermia?

A
  • Increased muscle activity
  • Inappropriate thermoregulation
  • Excited or stressed cats recovering from dissociative anesthetics
43
Q

What are the steps to recognition postoperative hyperthermia?

A
  • Routine monitoring of body temperature is important in avoiding damaging increases in body temp
  • Removal of external heating
  • Administration of tranquilizers, IVF, other therapies based on clinical signs and ongoing eval of patient usually prevent further progression of hyperthermia
44
Q

Can local anesthetics cause hyperthermia that is distinct from classical MH syndrome?

A
  • Excessive, toxic doses can cause inappropriate increases in body temperature through cortical stimulation and increased muscle tone
  • Seizure activity, as toxic SE of LA overdose, can further increase body temp