Hyperthermia
Mostly focusing on environmental exposure but if you’re looking for drug related there is a brief summary at the bottom
We are also not really going to look at fever as a cause.
In 2003 a heat wave killed over 1000 people in the UK. Causes of death range from dehydration related venous and arterial thrombus formation to heat stroke and the physiological stress being to much for particularly frail patients. This is demonstrated with the increased mortality persisting in the week after a heat wave as well as during it.
Heat stroke can be defined as a core (read rectal) temp over 40, but this isn’t everything.
Classical Heat Stroke is non exertional and is seen mostly in the elderly population but the very young are also vulnerable
Exertional Heat Stroke results from physical activity
There is also:
Heat Syncope – peripheral vasodilation causing collapse secondary to a high ambient temo
Heat Cramp – Muscle cramping occurring during exercise in heat, related ot salt deficiency and is benign
Heat Exhaustion – State of dehydration and weakness which accompanies exposure to extremes of heat.
Salt depletion heat exhaustion happens when an unacclimatised person exercise and only replace water loss
Water depleted heat exhaustion happens when they fail to replace water
Both lead to a state of electrolyte derangement and hypovolaemia
The clinical features are nausea, vomiting, weakness, lethargy headache and dizziness
There is preservation of consciousness, which distinguishes Exhaustion from Stroke
Heat Stroke - has a raised core temp with encephalopathy
Other features include coma, seizure, hot dry skin, hyperdynamic circulation, multi organ failure and DIC with rhabdomyolysis
Physiology
Human thermoregulation is both behavioral and autonomic.
The autonomic component;
- From the hypothalamus
- Sweating (through the latent heat of evaporation) and vasodilation
- Afferent type C nerve fibres conduct the sensation of heat to the hypothalamus (maximal firing at 45-50C)
- Received in the anterior hypothalamus, the posterior hypothalamus then coordinates the autonomic response
- Homeostatic point normal between 36.7 and 37.1. In this range there is no response from the hypothalamic effector neurons
o Diurnal variation by 1C
§ Greater variation throughout the menstrual cycle
o Range is also adjusted by anaesthesia to a 4 degrees of variance.
- Effector response is sweat production and cutaneous vasodilation
o Cardiac output increases by 20L/min
o Increase in cutaneous blood flow by 8L/min
o Evaporation of 1.7ml of sweat consumes 8kcal of energy, at maximal efficiency sweating can dissipate 600kcal/hr
The behavioural component is far more important – no amount of vasodilation or sweating will replace seeking a cooler environment.
Maximal sweat output is about 2L/hr – all this water and electrolytes (mostly NaCL) needs replacing.
Sustained heat exposure leads to break down of both behavioural and autonomic responses.
- Dehydration and fluid loss eventually gets to the point where you start conserving fluid, preventing sweating.
- Once you reach this stage, vasodilated skin becomes a risk – allowing for core temperature to equilibrate with the ambient temperature. Essentially becoming a big, efficient 2 way exchange surface.
How does this relate to heat stroke?
1. Failure of thermoregulation
a. Dehydration leads to impairment of cardiovascular response to heat – cardiac output doesn’t increase sufficiently
b. Leading to less sweat production
c. Skin gets hotter
d. Heat damage occurs to sweat glands and sweat production stops
e. Hot dry skin stops loosing heat and starts working to equilibrate with the surroundings (may still have a mild effect if ambient temperature low enough)
f. Progressing Hyperthermia
2. Direct Heat damage at a cellular level
a. If temperature reaches 49/50C then cellular necrosis will occur in <5mins
b. Cellular damage starts around 41.6-42C for 8hrs
3. Systemic Inflammatory Response
a. Heat stress causes cytokine release
b. Endothelial injury causing DIC and coagulopathy
c. Bacterial Translocation and endotoxaemia
On top of this cascade there is also though to be uncoupling of oxidative phosphorylation, enzyme failure and increased cell membrane permeability.
In organ systems heat stroke presents as following:
Respiratory Failure and ARDS – probably related to the SIRS, there is also a potential for pulmonary oedema that is non cardiac in origin
Cardiac, Electrolyte derangement and direct effect of heat can cause tachyarrhythmias, hypotension due to fluid loss and vasodilation and nitric oxide production
Neurological disturbance with delirium, lethargy, agitation, coma and seizure. The cerebellum is the most susceptible to damage and approx. 75% are left with long lasting neurological effects.
Lactic acidosis, respiratory alkalosis and electrolyte derangement (inc phosphate and calcium as they are deposited in the injured muscle)
Renal failure with rhabdomyolysis and myoglobin acute tubular necrosis
Hepatitis, well atleast elevated LFTs from muscle injury
DIC, possible from the endothelial injury? Maybe the endothelial glycocalyx plays a role (there is vasodilation and membrane break down with a SIRS response, it would make sense)
Contributory risk factors:
Enviormental
- High temp
- High humidity
- Low air movment
Patient
- Increased thermogenesis (exercise, hyperthyroid, sepsis)
- Decreased mobility or volition (ie not able to follow the behavior thermal regulation cues)
- Failure of normal thermoregulatory mechanisms (ie anticholinergics stopping you sweating)
- Male (women seem protected from exercise induced heat stroke, here is what I could find about this)
Protective Features (Acclimatisation)
Gradual adaption to increasing amounts of work in hot enviorments, takes weeks
- Increased cardiac output
- Renin-angiotensin-aldosterone activation
- Salt conservation by sweat glands (less salty sweat)
- Na retention by kidneys
- Increased capacity to sweat
- Plasma volume expansion
- Increased glomerular filtration rate to resist exertional rhabdomyolysis
Management of Heat Stroke
Goals – early aggressive cooling with organ support where needed
The aim is to get them cooled to below 38.5 (core) as soon as possible, prolonged cooling time is associated with poor outcomes.
Options for cooling the heat stroke patient:
- Evaporation of cold water sponges/ spraying with water and using a fan
- Ice packs
- Immersion in ice water
- Contact cooling by blankets and jackets
- Iced gastric, colonic, bladder, or peritoneal lavage
- Infusion of cold intravenous fluids
- Invasive technique such as cooling of the dialysis circuit, or ECMO
Liberal use of benzos prevent or reduces any shivering during cooling and helps with the agitation and would treat any seizure.
No role for dantrolene
3 conditions of being hot iatrogenically
- Malignant hyperthermia
- Genetic defect – uncontrolled release of calcium in skeletal muscle and uncoupling of oxidative phosphorylation
- Trigger (volatile anaesthetic agents, suxamthenonium)
- Jaw rigidity, high CO2, hyperthermia, tachycardia
- Dantrolene
- Neuroleptic Malignant Syndrome
- Neuroleptic drugs or sudden withdrawal of dopamine agonists
- Decreased dopamine activity in nigrostriatum and hypothalamus causes rigidity and altered thermoregulation
- Can occur at any time but more likely within 10 days
- Hot, confused, autonomic dusfunction (tachy, hypo/hypertension, diaphroesis,)
- Bromocriptine/dantrolene in severe cases, oven removal of source is sufficient
- Serotonin syndrome
- Excess serotonin in CNS and peripherally
- Commonest precipitants are venlafaxine, fluoxetine, citalopram, pethdine, tramadol
- Temp of 40 is common, mydriasis, hyperactive bowel sounds, diaphoresis with normal skin colour, clonus is an important finding (inducible, spont and ocular)
- Temor, diarrhoea, neuromuscular rigidity,
- Management
- Remove precipitant,
- 5ht antagonists (blocks post synaptic receptors)
- Benzos
- Physical restraint maybe counterproductive,
- Mostly supportive
- cyprohepatdine