BMS327
Transport accidents account for 13% of all traumatic injuries in Australia, what percentage of this is due to drugs and alcohol?
4.3% of transport accidents are accounted for due to drugs & Alcohol.
What percentage of of injuries requiring hospitalization are due to falls
40% of injuries requiring hospitalization are due to falls
How many people were severely injured and admitted to hospital during 2019
460,000 people
Of 460,000 people injured severely enough to be admitted to hospital, what percentage were males?
60% were males
hyperbaric chamber (week 6 module 3)
A chamber, usually a small room, pressurized to more than atmospheric pressure.
coagulopathy
A condition in which the blood's ability to clot is impaired
NOFF - NECK OF FEMUR FRACTURE
A fractured neck of femur (broken hip) is a serious injury, especially in older people. It is likely to be life changing and for some people life threatening. It occurs when the top part of the femur (leg bone) is broken, just below the ball and socket joint.
Brain atrophy
A general loss or deterioration of neurons in the cerebral cortex and limbic system.
Boyle's Law (week 6 Module 3)
A principle that describes the relationship between the pressure and volume of a gas at constant temperature: -Pressure and volume are inversely proportional as once increased the other decreases
Reperfusion and pressure 2nd effect as it pertains to crush syndrome: (week 9)
A second effect from pressure and reperfusion is the release of debris from the damaged cells into the circulation. (from nursing centre) This debris includes potassium, phosphorus, and myoglobin, the latter is responsible for the ARF that can occur with the syndrome. Myoglobin, an oxygen-binding molecule, contains a heme group and a globin group that disassociate into globin and ferrihemate when released into the circulation, especially in an acidic environment such as that of hypoperfusion. Myoglobin and myoglobin breakdown products, particularly in the presence of acidic urine (pH < 5.4), have a toxic effect on the renal tubules and react with the Tamm-Horsefall proteins in the renal tubules to form casts (Stewart, 2005). Recent literature implicates free radical formation as worsening cast-induced renal toxicity (Malinoski et al., 2004).
Definition of hypothermia (week 6 module 3)
A state of low body temperature, specifically a low CORE temperature < 35 C or < 95 F
Acute mountain Sickness - Therapeutic interventions (week 6 module 3)
ACS Therapeautic interventions - Acetaxolamide: Carbonic anhydrase inhibitor, aids ventilation acclimatisation to restore acid base balance caused by hyperventilation. - if not relieved by rest, descent is necessary - Specialized nonstandard medications: ie; Desamethasone.
Acute mountain sickness - Differential Diagnosis (week 6 module 3)
AMS differential diagnosis - Dehydration - Hypoglycaemia - intoxication or hangover or fatigue
Acidosis and Alkalosis
Acid-Base Imbalances Acidosis = pH < 7.35 greater acid than base Alkalosis = pH > 7.45 greater base than acid
High Altitude Pulmonary Edema (HAPE)
An altitude illness characterized by at least two of the following: dyspnea at rest, cough, weakness or decreased exercise performance, or chest tightness or congestion. Also, at least two of the following signs: central cyanosis, audible rales or wheezing in at least one lung field, tachypnea, or tachycardia.
What percentage of injuries requiring hospitalization are due to transport accidents?
Approximately 13% are. Injuries requiring hospitalization due to transport accidents
Pre-hospital "platinum 10 minutes"
- Assessment & Management. - Every action must have a life saving purpose. - Organised, detail-oriented, selective, rapid
Key elements of surviving trauma?
- Golden Period (formerly Golden Hour) - Pre-hospital "platinum 10 minutes"
Aetiology behind altitude related illness
- Hypoxia from reduced O2 pressure - fluid redistribution - Sympathetic activity - hypoventilation - cerebral oedema
Potential Injuries from barotraumas (week 6 module 3)
- Pneumothorax - Haemothorax - Tension Pneumothorax - Mediastinal emphysema - Arterial gas embolism - AMI - Stroke - Renal failure - Blindness
Drowing -Basics (week 6 module 3)
- Remove the patient from the water - Evaluate ABCs - Intitate ventilation. May be considered while the patient is still in the water - Suspect head and neck injury if the patient experienced a fall or was diving. - protect the patient from heat loss
Decompression Illness - Treatment (week 6 - Module 3)
- Transport at low altitude: Air transport may prove problematic as pressurised aircraft is generally required. - Give airway and ventilatory support, administer 100% oxygen - Replace fluids, correct dehydration if present - Conduct hyperbaric recompression
Altitude-Related Illness (week 6 module 3)
- sustained from decreasing pressure - lowering partial pressure of oxygen - unpressurized aircraft flight, mountain tracel - Most common in elevation >2666 metres or 8000 ft - symptomes may begin at 4000 ft or 1219 metres
Drowning Breathing (week 6 module 3)
- use continuous positive airway pressure (CPAP) if available. - If it is not available, consider early intubation, with appropriate use of PEEP Higher pressures may be required for ventilation because of the poor compliance resulting from pulmonary oedema or alveolar collapse
High Altitude Cerebral Oedema -HACE: Therapeutic interventions (week 6 - Module 3)
-Rapid descent is imperative -O2 -IV access -Dexamethasone
Golden period (formerly Golden Hour)q
-from moment of injury - to definitive treatment
Forms of Decrompression illness - Old terms (week 6 - Module 3)
1. "Creeps"= Skin manifestations 2. "Bends"= Joints 3. "Chokes"= Breathing 4. "Staggers" = Neurological / Spinal
How many deaths are due to injury?
12,000 or 8% of all deaths are due to injury.
osmotic
_O_ __ __ __ __ __ __ pressure is caused by water inside a plant cell pushing against the cell wall.
bronchospasm
a contraction of the smooth muscle in the walls of the bronchi and bronchioles that tighten and squeeze the airway shut
Dysbarism
a medical condition that results from pressure changes that occur when a person descends in water or ascends in altitude
nitrogen narcosis (week 6 module 3)
a physiological condition caused by an increased partial pressure of nitrogen, resulting in symptoms similar to those of intoxication
anoxia
absence of oxygen
Compartment Syndrome as it pertains to crush syndrome: (week 9)
another complication of crush injuries is the development of compartment syndrome, (from nursing centre) which occurs when pressures increase within a fascia-encased region, classically a muscle group or the abdomen. The fascia provides a nonexpandable space, and, as fluid is sequestered, the pressure within the compartment rises. With the rise in pressure, the microvascular circulation is compromised leading to tissue ischemia. The signs and symptoms of compartment syndrome in an extremity include pain out of proportion to the injury or with passive motion, pallor, paresthesia, pulselessness, and paralysis of the affected extremity. Attempts should be made to intervene before there is a loss of pulses, an ominous finding that will almost always reflect irreversible tissue necrosis. Compartment syndrome may also occur in the abdomen. To monitor abdominal compartment syndrome, bladder pressures may be obtained through an indwelling urinary catheter. Pressures higher than 25 mmHg often warrant surgical decompression.
peri-oral cyanosis (week 6 module 3)
blue around the lips
BCR
bulbocavernosus reflex The bulbocavernosus reflex indicates the absence or presence of spinal shock. Spinal shock usually occurs between 24 and 72 hours after spinal injury. Spinal shock is manifested by the absence of bulbocavernosus reflex, hypotension, bradycardia, and complete loss of motor, sensation and reflexes.
Causes of obstructive shock
cardiac tamponade, tension pneumothorax, pulmonary embolism are causes of?
hypocapnia
condition of deficient carbon dioxide (in the blood)
Triad of heat Stroke (week 6 module 3)
Defined by a triad of: 1. Core temperature higher than 40.5° C 2. Hot, Dry Skin 3. Altered mental status
Two types of dysbarism
Direct Dysbarism:- Expansion of gases within body cavities Indirect Dysbarism:- Decompression illness - gas coming out of solution
Fresh Water Drownings (week 5 module 3)
Fresh water washes away surfactant - alveoli collapse... Ventricular fibrillation usually occurs
Pilorection
Goose bumps or goose flesh
High Altitude Pulmonary Oedema -HAPE- Aetiology (week 6 - Module 3)
HAPE aetielogy - Fluid Buildup prevents oxygen and CO2 exchange - Hypertension - Hypoxia - Hypo-perfusion - Impaired cerebral function - Death remember; hypocapnia cause vasoconstriction
High Altitude Cerebral Oedema -HACE - Aetiology (week 6 - Module 3)
High Altitude Cerebral Oedema -HACE - Aetiology -Excessive fluid leakage and swelling of the brain -Increased intracranial pressure -Occurs after 1-3 days at altitude -Most often occurs at >4000m (12,000') - Hypoxia (at high altitudes due to the reduced p02 ie; the higher you go the less O2 that is available) --> inflammatory response --> causes cerebral vasodilation --> increase ICP --> cerebral hypertension --> over perfusion --> increased capillary pressure/leakage --> cerebral oedema. -
High Altitude Cerebral Oedema -HACE: Differential Diagnosis (week 6 - Module 3)
High-altitude cerebral oedema: Differential diagnosis -CVA -Hypoglycaemia -Other metabolic derangements -Intoxication -Fatigue
High Altitude Cerebral Oedema -HACE: Physical Findings (week 6 - Module 3)
High-altitude cerebral oedema: Physical findings -Disorientation -Severe headache -Ataxia -Decreased LOC -Drowsiness not relieved by rest -Hallucinations -Confusion -Stupor -Coma
High Altitude Pulmonary Oedema -HAPE: Differential Diagnosis (week 6 - Module 3)
High-altitude pulmonary oedema: Differential diagnosis -Pneumonia -Infection -Fatigue -Cardiogenic and non-cardiogenic pulmonary edema -Hypoxia -Hypoglycaemia -Metabolic disorders
High Altitude Pulmonary Oedema -HAPE: Therapeutic interventions (week 6 - Module 3)
High-altitude pulmonary oedema: Therapeutic interventions -Primary treatment is descent -O2 -Specialized nonstandard Pre-Hospital medications Nifedipine (Adalat)
High Altitude Pulmonary Oedema -HAPE- Physical findings (week 6 - Module 3)
High-altitude pulmonary oedema; Physical findings -Persistent wet cough, producing white, watery, frothy fluid -Crackles for breath sounds -Inability to sleep -Inability to lay supine without sensation of suffocation -Dyspnoea -Tachypnoea -Lethargy -Irritability, confusion, disorientation -Coma
hyperemesis
Hyperemesis gravidarum (HG) is a severe form of nausea and vomiting, associated with dehydration, ketonuria and weight loss. HG affects 0.3-3.6 per cent of all pregnancies. It has emotional, physical and economic consequences for women and can lead to adverse outcomes such as low birth weight.
Is Hypotension a compensated (early) sign of shock?
Hypotension is a late sign of shock
How many times are indigenous Australians likely to be admitted to hospital?
Indigenous Australians were twice as likely to be admitted to hospital
Barotrauma
Injury resulting from pressure disequilibrium across body surfaces; for example, from too much pressure in the lungs.
Heat Stroke Metobolic breakdown (week 6 module 3)
Metabolic breakdown, irreversible organ death at 43° C •"Critical thermal maximum" •Cellular respiration impaired •Increased cellular membrane permeability •Enhanced heat production •Protein denaturing •Tissue necrosis •Rhabdomyolysis, pulmonary oedema, renal failure, cardiac dysfunction
High Altitude Cerebral Oedema -HACE (week 6 - Module 3)
Most severe altitude injury causing intracranial pressure from swelling
Boyle's Law Equation (week 6 module 3)
P1V1 = P2V2
Pathophysiology of Crush injuries (week 9)
Pahthophysiology of crush injuries: -Traumatic rhabdomyolysis. -Hypovolemia -Reperfusion injury -Compartment Syndrome
Prevention of high-altitude illness
Prevention of high-altitude illnesses •Many strategies •Generally, slow ascents with rest periods and acclimation
Pulmonary Barotraumas - Managment (week 6 module 3)
Pumonary barotraumas - treat underlying injury - Address ABCs - Conduct hyperbaric therapy
Return of circulation - Reperfusion injury as it pertains to crush syndrome: (week 9)
Return of circulation to the injured and ischemic area after rescue also results in injury, as reperfusion leads to increased neutrophil activity and the release of free radicals. Superoxide, the anion form of oxygen (O2-) and hydrogen peroxide (H2O2) react to form the hydroxyl radical ([middle dot]OH), which, in a large enough concentration, damages cellular molecules and causes a lipid peroxidation. Lipid peroxidation leads to cell membrane destruction and cell lysis (Civetta, Taylor, & Kirby, 1997). This damage leads to a further increase in the absorption of fluid, calcium, and sodium into the damaged cells. The amount of fluid that may be rapidly sequestered in the injured muscle can be equal to the extracellular volume of the patient, about 12 L in a 75-kg adult (Stewart, 2005).
Saltwater Drownings (week 6 module 3)
Salt water draws fluids from bloodstream and pulmonary oedema occurs - Start pulmonary resuscitation immediately
pulmonary barotraumas (week 6 module 3)
Secondary to inadequate exhalation during ascent Expansion of gas in Lungs ruptures pulmonary tissue
Altitude-related illness - Severe Acute Mountain Sickness - presentation (week 6 module 3)
Severe AMS - Severe weakness - Severe, protracted vomiting - Decreased urine output - Resting dyspnoea - Altered LOC - Cough and congestion - Inability to walk Straight line/ataxia - Pale or changing skin colour
obstructive (mechanical) shock
Shock that occurs when there is a block to blood flow in the heart or great vessels, causing an insufficient blood supply to the body's tissues.
Clinical Features of crush syndrome/crush injury: (week 9)
Some or all of the following clinical signs and symptoms may be present: (from nursing centre) Cardiovascular instability Hypotension and hypovolemic shock. This may be caused from the massive fluid shift from the extracellular fluid space into the damaged cell s or associated injuries causing blood loss. Arrhythmia and negative inotropy secondary to hyperkalemia, hypocalcemia and hyperphosphatemia Cardiomyopathy Renal failure Secondary to circulatory shock and intravascular volume depletion leading to renal cortical ischemia. Release of myoglobin, urate, phosphate and purine by the muscle cells causes precipitation in the distal convoluted tubules, causing tubular obstruction. Metabolic acidosis with lactic acidosis Disseminated intravascular coagulopathy Hypothermia Myoglobinuria Skin injury and swelling Paralysis and paresthesia Pulses may or may not be present. Compartment syndrome Acute lung injury / ARDS
anoxia/hypoxia
Specifically, anoxia is a condition in which there is an absence of oxygen supply to an organ's tissues although there is adequate blood flow to the tissue. Hypoxia is a condition in which there is a decrease of oxygen to the tissue in spite of adequate blood flow to the tissue.
mild hypothermia -temperature range (week 6 module 3)
Temperature range of mild? 32 and 35°C SIGNS & Symptoms •Lethargy / Apathy •Shivering •Lack of Coordination •Pale, cold, dry skin •Early rise in blood pressure, heart, and respiratory rates. Active Rewarming of MILD Hypothermia: Active external methods: -Warm blankets -Heat packs -Warm water immersion (with caution) - Active internal methods: - Warmed IV fluids
Moderate hypothermia -temperature range (week 6 module 3)
Temperature range of moderate? 29 and 32°C Signs & symptoms: •No shivering •Altered mental status •Muscular rigidity •Bradycardia Hypotension
Bulbocavernosus reflex BCR
The bulbocavernosus reflex indicates the absence or presence of spinal shock. Spinal shock usually occurs between 24 and 72 hours after spinal injury. Spinal shock is manifested by the absence of bulbocavernosus reflex, hypotension, bradycardia, and complete loss of motor, sensation and reflexes.
Traumatic rhabdomyolysis, as it pertains to crush syndrome: (week 9)
Traumatic rhandomyolysis as it pertains to crush syndrome, (from nursing centre) results when muscle mass is compressed, causing direct injury to muscle fibers. As the tissue is compressed, it is deprived of blood flow and becomes ischemic, eventually leading to cellular death. The time to injury and cell death varies with the crushing force involved; however, skeletal muscle can often tolerate ischemia for up to 2 hr without permanent injury. In the 2- to 4-hr range, some reversible cell damage occurs, and by 6 hr irreversible tissue necrosis generally sets in. In addition to ischemic cell damage, direct injury from the crushing forces causes cell membrane failure and the opening of intracellular sodium and calcium channels. The opening of these channels results in the shift of calcium and sodium into hypoxic cells. This damages myofibril proteins and results in both worsened cell membrane dysfunction and the release of ATP-inhibiting nucleases. The resultant pressure-induced reduction in aerobic metabolism is further compounded by the ischemia of reduced blood flow.
PEEP valve
Valve that is attached to the exhalation port of the patient's valve in order to hold a positive expiration pressure at the patient's mouth at the end of the expiratory phase
Drowning - Aetiology (week 5 Module 3)
Water intake hits posterior oropharynx - Laryngospasm - Bronchospasm - Severe hypoxia - Acidosis - Cardiac Disturances - CNS anoxia - Coma
pulse pressure
difference between systolic and diastolic pressure
hyperbaric oxygen therapy = HBOT (week 6 module 3)
involves breathing pure oxygen in a special chamber that allows air pressure to be raised up to three times higher than normal
MAP
mean arterial pressure MAP <40 = Brain Damage MAP of 50 = minimum target MAP of 65 = heart perfusion MAP of 65-75 Kidney Perfusion
hyperbaric medicine (week 6 module 3)
medicinal use of high barometric pressure to increase oxygen content of blood and tissues
Acute Mountain Sickness (AMS)
most common altitude illness - 30% of people exposed to moderate altitude >3500 metres
peep
positive end expiratory pressure
pulmonary surfactant (week 6 - Module 3)
surface active agent: secreted fluid by the alveolar cells: reduces surface tension of pulmonary fluids: contributes to the elasticity of the lung: prevents lung fillage h2o (infants)
TXA (tranexamic acid)
synthetic amino acid lysine that prevents the breakdown of clots to stop the bleeding
laryngospasm
the sudden spasmodic closure of the larynx
TBI
traumatic brain injury
Heat Stroke Management (week 6 module 3)
•Support ABCs •Rapid cooling (0.1°C/minute is achievable) •Replace fluids and electrolytes •Give fluids judiciously •Hypotension may correct once peripheral vasoconstriction occurs with cooling •Monitor hydration •Urine output •Skin colour and condition •Blood pressure
Rhabdomyolysis - Tests (week 9 - crush injuries)
(Tests of Rhabdomyolysis): - Positive myoglobin - High CPK (Creatine phosphokinase (CPK)) - High Potassium - Urinalysis positive for haemoglobin and/or myoglobin
Rhabdomyolysis - Symptoms of (week 9 - crush injuries)
(Symptoms of Rhabdomyolysis:) - Dark or red urine. - General weakness. - Muscle stiffness of aching. - Muscle tenderness or weakness
Treatment of cardiogenic shock
"Identify cause. Give pressors (dopamine - Dobutamine)" In addition to ensuring the patient is adequately oxygenated, It should be understood that the primary goals in pharmacologic management of cardiogenic shock are restoration of oxygenated blood flow in conjunction with a reduction of cardiac workload and cardiac oxygen consumption. Nitroglycerin is a potent coronary vasodilator and a peripheral vasodilator that has proved to be highly beneficial when used in patients with cardiogenic shock.
Hyperkalemia - causes (week 9 - Crush injuries)
(Causes of Hyperkalemia) 1. Increased K (potassium) intake (IV or Oral) - Transfusion (PRBC). 2. Transcellular shift, H ions enter and decrease cellular uptake of K - Crush injury, rhabdomyolysis, tumours, medications, succinylcholine, beta blockers, haemolysis. 3. Decreased K excretion = Renal failure
Rhabdomyolysis causes (week 9 - crush injuries)
(Causes of Rhabdomyolysis:) 1. Trauma 2. Prolonged immobility (ischemia or necrosis of Muscle (DVT) 3. Snake bites 4. Seizures 5. Crush injuries 6. Heat stroke 7. Severe exertion such as marathon running 8. Severe electric shock.
Hyperkalemia - definition (week 9 - Crush injuries)
(Definition of Hyperkalaemia) Is defined as a potassium level greater than 5.5 mEg/L - 5.5-6.0 mEg/L = Mild - 6.1-7.0 mEq/L = Moderate - 7.0 mEq/L and greater = Severe
Rhabdomyolysis - Definition (week 9 - crush injuries)
(Definition of Rhabdomyolysis): Breakdown of muscle fibres resulting in the relase of myoglobin into the bloodstream. Frequently result in kidney damage
How to calculate MAP
(SBP + 2DBP)/3 so 120/80 would = 120 + 160 = 280 / 3 = 93 MAP
CPK (creatine phosphokinase) (week 9 - Crush Injuries)
CPK is creatine phosphokinase, and enzyme that is released during and after intense muscle activity normal levels of K are 3.5 to 5mmol/l in most laboratory settings
Crush Syndrome V Compartment syndrome (week 9 - from orthopaedic trauma)
Compartment syndrome and crush syndrome are two closely related clinical entities. Both arise as a consequence of trauma to muscle, which results in swelling and a compromised circulation to muscles and nerves at the microvascular level. If reperfusion of the tissue isn't restored as quickly as possible, then tissue ischaemia may culminate in cell death and the crippling wholesale loss of muscle compartments. It may be useful to think of compartment syndrome in terms of a localised problem within an osteo-fascial muscle compartment. This is characterised by relentlessly worsening pain in the injured limb. The only effective treatment is fasciotomy which decompresses the ischaemic muscle, allowing it to be reperfused and so rescuing it from death. Fasciotomy is an emergency procedure! Crush syndrome may arise as a result of a neglected compartment syndrome or directly from severe injury. In crush syndrome the products of muscle cell damage lead to systemic problems which manifest as hyperkalaemia, acidosis, myoglobinuria, and renal failure. When a patient is freed from limb entrapment, reperfusion initiates this process; the most urgent danger is from hyperkalaemia leading to cardiac dysrhythmias and sudden death. Amputation can be life-saving if there are no means or resources to medically manage the hyperkalaemia and later renal failure. The decision whether to perform fasciotomies in crush syndrome is determined by the duration of ischaemia. If this is greater than 6-8 h, the muscle will not be rescued. The patients' compartments should be left closed, provided the life-threatening metabolic consequences of hyperkalaemia and myoglobinuria can be managed medically. If not, amputation should be performed swiftly.
Crush Syndrome (week 9)
Crush Syndrome is the systemic manifestation of muscle cell damage resulting from pressure or crushing.(from nursing centre) Initially described by Bywaters and Beall in 1941in a patient who initially appeared to be unharmed but subsequently died of renal failure. Crush Syndrome: Crush injury with systemic manifestations. Systemic manifestations are caused by a traumatic rhabdomyolysis due to muscle reperfusion injury when compressive forces on the tissues are released.This can cause local tissue injury, organ dysfunction, and metabolic abnormalities, including acidosis, hyperkalemia, and hypocalcemia.
Aeitology of crush injuries (week 9 - Crush injuries)
Crush injury A crush injury occurs when force or pressure is put on a body part. This type of injury most often happens when part of the body is squeezed between two heavy objects. Damage related to crush injuries include: Bleeding Bruising Compartment syndrome (increased pressure in an arm or leg that causes serious muscle, nerve, blood vessel, and tissue damage) Fracture (broken bone) Laceration (open wound) Nerve injury Infection (caused by bacteria that enter the body through the wound)
Hypovolemia, as it pertains to crush syndrome: (week 9)
Crush injury also causes hypovolemia by hemorrhagic volume loss and the rapid shift of extracellular volume into the damaged tissues.(from nursing centre) Acute renal failure (ARF) is caused by hypoperfusion of the kidneys, which normally receive 25% of cardiac output (Lameire, 2005). This hypoperfusion compounds the toxicity caused by cast formation and mechanical blockage of the nephrons by myoglobin, and underscores the importance of early, vigorous volume resuscitation to improve urine flow, which dilutes and clears toxins.
Key Management points of Crush Syndrome; Crush Injury (week 9)
Key management points (from cancer therapy advisor) Primary survey with focus on airway, breathing and circulation. Establishing intravenous access and initiation of fluid resuscitation prior to releasing the crushed extremity, especially if the time of entrapment is > 4 hours. If extrication is impossible short-term use of tourniquet on the affected limb is recommended until intravenous access can be obtained. Acute limb amputation should be avoided until extrication is impossible. Continue with fluid resuscitation while transfer to a medical facility is initiated. Monitor the crushed limb for the 5 P's: Pain, Pallor, Paresthesia, Pain with passive movement and Pallor. Combat hypotension with aggressive hydration. Prevention of renal failure is important. Alkaline diuresis and mannitol therapy is recommended. Hemodialysis is also recommended for acute renal failure. Electrolyte abnormalities (hypokalemia / hypocalcemia / hyperphosphatemia) need to be monitored and treated accordingly. Monitoring for cardiac arrhythmia is recommended. Correction of acidosis with alkalinization of the urine is critical. Monitoring for compartment syndrome is also recommended. If present it should be treated with fasciotomy. Fasciotomies should not be performed if the compartment syndrome has been present for > 24 hours. Open wounds should be treated with antibiotics, tetanus toxoid and debridement of necrotic tissue. Hyperbaric oxygen therapy may be useful.
Hypoxia
Low oxygen saturation of the body, not enough oxygen in the blood
Altitude-related illness - Mild Acute Mountain Sickness - presentation (week 6 module 3)
MILD AMS - Mild Headache - Lightheadedness and dizzyness - Difficulty Sleeping - Loss of appetite - Breathlessness - Fatigue - Nausea and vomiting
