Prof. Sevda Özdoğan

SPECİAL PULMONARY PROBLEMS

Defi ne fatal and nonfatal drowning Explain the mechanism of drowning and end organ eff ects List the management needs in near drowning and factors that

cause poor prognosis Defi ne barotrauma and types of formation Explain the complications of barotrauma Explain the mechanism of arterial gas embolism and list the

syptoms Explain the mechanism of decompression sickness List the symptoms and treatment approach in decompression

sickness Defi ne nitrogen narcosis and risk of it Defi ne the mechanism and clinic of high altitude illness List the symptoms and risk factors of high altitude disease List the preventive measures of high altitude disease

LEARNİNG OBJECTİVES

Drowning

Underwater dangers Barotrauma, Decompression sickness, Scuba diving Nitrogen narcosis

High altitude illness

Every year, drowning accounts for at least 500,000 deaths worldwide, Statistics for nonfatal drowning are more diffi cult to obtain, but nonfatal drowning events may occur several hundred times as frequently as reported drowning deaths

Fatal Drowning: Death that occurs within 24 hours of submersion in a

liquid medium

Nonfatal Drowning: Survival, at least temporarily, after suff ocation by

submersion in a liquid medium“A process resulting in primary respiratory impairment from submersion or immersion in a liquid medium”

DROWNİNG

Fatal and nonfatal drowning typically begins with a period of panic, loss of the normal breathing pattern, breath-holding, air hunger, and a struggle by the victim to stay above the water.

Reflex inspiratory eff orts eventually occur, leading to hypoxemia by means of either aspiration (wet nonfatal drowning) or reflex laryngospasm (dry nonfatal drowning) that occurs when water contacts the lower respiratory tract.

Hypoxemia in turn aff ects every organ system, with the major component of morbidity and mortality being related to cerebral hypoxia

Formerly, the distinction between salt water and fresh water drowning was emphasized:

It was believed that the hypertonicity of salt water caused plasma to be drawn into the pulmonary interstitium and alveoli, leading to massive pulmonary edema and hypertonic serum.

Drowning in fresh water was thought to create the opposite effect, with aspirated hypotonic fluid rapidly passing through the lungs and into the intravascular compartment, leading to volume overload and dilutional effects on serum electrolytes

Aspiration of more than 11 mL/kg of body weight must occur before blood volume changes occur, and more than 22 mL/kg before electrolyte changes take place which is unusual for nonfatal drowning victims to aspirate more than 3 to 4 mL/kg,

Decreased lung compliance,

Ventilation-perfusion mismatching,

Intrapulmonary shunting, leading to hypoxemia

Diffuse organ dysfunction

The temperature of the water and the presence of contaminants may affect patient outcomes

RESULTS OF BOTH TYPES OF DROWNİNG

Pulmonary Hypoxemia Washout sulfactant (anoxic degradation, inactivation) Noncardiogenic pulmonary edema Aspiration of gastric content ARDS

Neurological Hypoxemianeuronal damage Cerebral edema İncrease in intracranial pressure

END ORGAN EFFECTS

Cardiovascular Arrhythmias secondary to hypothermia and hypoxemia

Acid base and electrolites A metabolic and/or respiratory acidosis is often observed Severe electrolite changes rarely due to swallowed extremely

concentrated seawater

Renal Failure rarely due to acute tubular necrosis resulting from

hypoxemia,

Coagulaton Hemolysis and coagulopathy are rare

Prehospital care Ventilation (two rescue breathing), resuscitation Injury stabilization Postural drainage techniques to remove water from the lungs

are of no proven value Oxygen supplementation Rewarming hypothermic patients Arrhythmias require no immediate treatment

Emergency department care Frequent vital sign measurements and clinical reassessment Immediate intubation if:

Signs of neurologic deterioration or inability to protect the airway Inability to maintain a PaO2 above 60 mmHg or oxygen saturation

(SpO2) above 90 percent despite high-flow supplemental oxygen PaCO2 above 50 mmHg

MANAGEMENT

supplemental oxygen NIMV Nasogastric decompression Glucose measurement Trauma evaluation Rewarming Continue resustation (for several hours) in hypotermic

patients Symptomatic patients in good condition should be

monitorized until the symptoms and physiologic disturbances resolve

Hospital care

Factors that cause poor prognosis:

Duration of submersion >10 minutes Time to effective basic life support >10 minutes Resuscitation duration >25 minutes Water temperature >10ºC (50ºF) Age <3 years Glasgow coma scale <5 (comatose) Persistent apnea and requirement of cardiopulmonary

resuscitation in the emergency department Arterial blood pH <7.1 upon presentation

UNDERWATER DANGERS

Emergencies specifi c to diving:

Barotrauma, including arterial air embolism Decompression sickness Nitrogen narcosis

Two basic gas laws:

Boyle's law: At a constant temperature, the volume of a gas varies inversely with the pressure to which it is subjected. This law helps to explain the principles behind diving-related barotrauma and air embolism.

Henry's law: At a constant temperature, the amount of a gas that is dissolved in a liquid is directly proportional to the partial pressure of that gas. This law provides the explanation for decompression sickness and nitrogen narcosis.

Barotrauma occurs when an air fi lled area fails to equilibriate its pressure with the environmental changes of pressure

During descent, decreasing air volume in a space that also contains tissue leads to mucosal edema, vascular engorgement, and hemorrhage.

During ascent !!, increasing gas volume in a confined space can produce tissue disruption and rupture.

BAROTRAUMA

The second leading cause of death among scuba divers

As a diver descends, the air in the lungs becomes compressed. Pulmonary edema and hemorrhage occur when lung volume decreases below residual volume

As a diver ascends and transalveolar pressure exceeds 20 to 80 mmHg, overexpansion injury in the form of alveolar rupture can occur

PULMONARY BAROTRAUMA

Following alveolar rupture, gas can dissect along the perivascular sheath into the mediastinum to produce pneumomediastinum: a sensation of fullness in the chest, pleuritic chest pain that may radiate to the shoulders, dyspnea, coughing, hoarseness, Dysphagia Crepitation in the neck due to associated subcutaneous

emphysema Pneumothorax

PNEUMOMEDİASTİNUM

Spontaneous pneumotorax is rare (10%) History of spontaneous pneumothorax, bullae, or cystic

lung disease increase the risk If this occurs at a signifi cant depth, the pleural gas

expands as the diver ascends and can result in a tension pneumothorax dyspnea, chest pain, tachycardia, hypotension, cyanosis, distended neck veins, hyperresonance to percussion, unilateral decrease in breath sounds, Accompanying subcutaneous emphysema (25%)

PNEUMOTHORAX

Ear barotrauma: Pressure in the middle ear normally equilibrates with ambient pressure via the eustachian tube. However, if upon descent this equalization is prevented by mucosal edema secondary to an upper respiratory infection, pregnancy, or anatomic variations, the negative pressure in the middle ear can lead to its fi lling with serous fluid or blood or to inward rupture of the tympanic membrane

Sinus barotrauma

Dental barotrauma

The most serious potential sequel of pulmonary barotrauma

Mechanism:

Passage of gas bubbles into the pulmonary veins and from there into the systemic circulation

Development of venous gas emboli (either from barotrauma or decompression sickness), which overwhelm the filtering capacity of the pulmonary capillaries to appear in the systemic arterial circulation

Development of venous gas emboli that reach the arterial circulation "paradoxically" via a functional right-to-left shunt, such as a patent foramen ovale

ARTERİAL GAS EMBOLİSM

After reaching the systemic arterial circulation, gas emboli typically break up and produce distal ischemia and local activation of inflammatory cascades.

The specific symptoms and signs produced are dependent upon the final location of gas emboli; the most serious clinical consequences occur with embolization to the cerebral and coronary arteries

arrhythmias, myocardial infarction, and/or cardiac arrest

Focal motor, sensory, or visual deficits to seizures, loss of consciousness, apnea, and death.

Cyanotic marbling of the skin and focal pallor of the tongue.

Embolization to the kidney can produce hematuria, proteinuria, and renal failure.

Uterine and gastrointestinal bleeding and failure of other organs have occasionally been reported.

As a diver descends and breathes air under increased pressure, the tissues become loaded with increased quantities of oxygen and nitrogen as predicted by Henry's law. As the diver returns to the surface, the sum of the gas tensions in the tissue may exceed the ambient pressure and lead to the liberation of free gas from the tissues in the form of bubbles;

The location of bubble formation is somewhat dependent upon tissue characteristics.

The liberated gas bubbles can alter organ function by blocking vessels, rupturing or compressing tissue, or activating clotting and infl ammatory cascades.

Any intracardiac right-to-left shunt (eg, PFO, ASD, VSD) increases the risk of paradoxical air emboli, and is considered by many to be a contraindication to continued diving

DECOMPRESSION SICKNESS

SCUBA TANK

Approximately 75 percent of patients with decompression sickness develop symptoms within one hour and 90 percent within 12 hours of surfacing; only a small number become symptomatic more than 24 hours after diving.

Scuba divers should wait 12 to 48 hours before flying on a commercial airliner, depending upon the length of their diving exposures, to avoid decompression sickness in a diver who has subclinical gas bubbles

Mild form: Localised joint pain (elbow, shoulder most common) Skin pruritus (air bubbles in the skin), localised erythema,

cyanosis Lymphatic obstruction by bubbles, although rare, can lead

to pain, lymphadenopathy, and localized edema

Severe decompression: Nervous system involvement: damage to the spinal cord

Paresthesia, weakness, paraplegia, loss of syphincter control Pulmonary involvement:

wheezing, dyspnea, and pharyngeal irritation Right hearth failure, circulation collapse, death

SYMPTOMS

Administration of 100 percent oxygen,(increased o2 in circulation increases the nitrogen gradient between the gas bubbles and circulation which accelerate the reabsorbtion of gas bubbles)

Hyperbaric oxygen therapy

Positioning the patient in the left lateral decubitus and mild Trendelenburg or supine position in an eff ort to restore forward blood fl ow with caution for cerebral edema

Hydration (decrease vascular collaps, maintain collateral fl ow)

Complete resolution of the symptoms is seen in 75% even in the severe form if the treatment if started immediately

TREATMENT

Nitrogen narcosis is caused by the raised partial pressure of nitrogen in nervous system tissue, and usually occurs at depths greater than 30 m.

It induces signs and symptoms similar to alcohol or benzodiazepine intoxication, such as impairment of intellectual and neuromuscular performance and changes in behavior and personality.

Hallucinations and loss of consciousness can occur at depths greater than 90-91 m.

Divers recover rapidly upon ascent to a shallower depth. The main danger of this condition stems from impairment of the diver's judgment, which can lead to drowning accidents.

NİTROGEN NARCOSİS

High Altitude illness is the collective term for the unique cerebral and pulmonary syndromes (HACE/HAPE) that can occur following an initial ascend to high altitude or following a further ascend while already at high altitude

Induced by the hypoxic stress of high altitude and characterised by extravascular fluid accumulation in the brain and lungs

HIGH ALTITUDE ILLNESS (HAI)

Barometric pressure (Pb) diminishes exponentially with increasing altitude, Diminished PIO2 at altitude is the direct result of lower barometric pressure. As PIO2 decreases, so does the partial pressure of alveolar oxygen (PAO2), arterial PO2 (PaO2), and arterial oxygen saturation (SpO2), resulting in tissue hypoxia. This form of hypoxia is termed hypobaric hypoxia, and it represents the initial cause of high altitude illness. it becomes physiologically significant at elevations over approximately 2500 m.

The normal compensatory responses to acute hypobaric hypoxia are termed acclimatization,

An incompletely understood, complex series of physiologic changes involving multiple organ systems that occurs over varying periods (from minutes to weeks).

Acclimatization reduces the gradient between PIO2 and tissue PO2, thus optimizing the delivery and utilization of oxygen at the cellular level.

The fi rst and most important step in improving oxygen delivery is an increase in ventilation. Without increased ventilation, humans could not tolerate altitudes higher than 5000 m

As ventilation rises in response to hypoxia, PaCO2 falls and pH rises. The central chemoreceptors in the medulla of the brain respond to alkalosis in the cerebral spinal fluid (CSF) by inhibiting ventilation, such that the full hypoxic ventilatory response is attenuated.

Partial renal compensation for respiratory alkalosis occurs within 24 to 48 hours of ascent as the kidneys excrete bicarbonate, decreasing the pH toward normal, and allowing ventilation to again increase as the alkalosis is reduced. Plasma bicarbonate concentration continues to drop and ventilation to rise with further increases in altitude.

increased sympathetic activity transiently increases cardiac output, blood pressure, heart rate, and venous tone.

The pulmonary vasculature constricts in response to hypoxia, resulting in prompt, but highly variable increases in pulmonary vascular resistance and PA pressure

Following rapid ascend: Headache Fatique, lightheadedness Anorexia Nausea, vomiting Sleep disturbances (altered breathing in nonREM sleep) Shorthness of breath with exertion Nonproductive coughpink frothy sputum of pulmonary edema Diffi culty in walking up the hilldyspnea at rest Retinal hemorrhage

(HAPE symptoms typically appear 2-4 days after arrival at a new altitude)

SYPTOMS

Individual susceptibility (unexplained failure in acclimatization)

Past history of HAI

Rate of ascend

Vigorious exertion prior to acclimatization

Alcohol, sedatives eg substances interfere with acclimatization

Comorbidities

RISK FACTORS

Gradual ascend

Education

Alcohol and certain drug avoidance

Diet and hydration should be carefully supervised

Exertion limitation

Pharmacologic prophylaxis (acetazolamide, dexamethasone)

PROPHYLAXIS

END