Prof. Sevda Özdoğan2013

SPECİAL PULMONARY PROBLEMS

Drowning

Decompression sickness, Barotrauma, Scuba diving

Acute Mountain sickness, high altitude problems

Exposure to chemical weapons

Smoke injury

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 or reflex laryngospasm 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

DECOMPRESSİON SİCKNESS, BAROTRAUMA, SCUBA DİVİNG

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.

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

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

dysrhythmias, 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.

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

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.

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

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

DECOMPRESSION SICKNESS

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 Skin pruritus, 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

HydrationAdministration of 100 percent oxygen, Positioning the patient in the left lateral decubitus

and mild Trendelenburg (bed angled downward toward head) position in an eff ort to restore forward blood flow

Hyperbaric oxygen therapy

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: 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 signifi cant at elevations over approximately 2800 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.

ACUTE MOUNTAİN SİCKNESS

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 brain respond to alkalosis 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 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. Heart rate remains elevated while stroke volume is diminished due to decreased plasma volume

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

Cerebral blood flow increases in response to hypoxemia that cause headache and high altitude cerebral edema

Periodic breating at nonREM sleep occurs due to hypoxemia and hypocapnia

HeadacheFatigueLightheadednessAnorexiaNauseaVomitingdisturbed sleep with frequent awakeningmild shortness of breath with exertion.

Symptoms may be mild or severely debilitating.

SYMPTOMS OF AMS

 High altitude cerebral edema (HACE) generally occurs in individuals with acute mountain sickness (AMS) and/or high altitude pulmonary edema (HAPE) at elevations over 3000 to 3500 m. The hallmarks of HACE are encephalopathic symptoms and signs, including ataxia, severe lassitude, and progressive decline of mental function and consciousness (irritability, confusion, impaired mentation, drowsiness, stupor, and finally coma).

Patients with HAPE manifest pulmonary findings, such as crackles, breathlessness

Acute Mountain Sickness

Treatment of AMS is based upon symptom severity and, in mild cases, patient preference

Supplemental oxygen Avoid further ascend Limit physical activity Avoid alcohols eg Basic analgesics for headache and antiemetics Occasionaly descent Acetozolamide increase the acclimatization Dexamethazone

TREATMENT

High altitude cerebral edema Descent is the definitive treatment. Dexamethasone supplemental oxygen, hyperbaric therapy

Gradual ascent should be emphasized

Nerve agents (cholinesterase inhibitors) The prototypical nerve agent is sarin. Exposure can occur via the lungs, skin, or eyes. Nerve agent weapons are transported in liquid form and transform into

gas upon release due to their volatility. The mechanism of action is inhibition of cholinesterase, which produces a

state of acetylcholine excess. The resulting excessive cholinergic activity produces severe secretions from many sites and stimulation of smooth muscle.

Nerve agents inhibit nerve transmission in skeletal muscle; this affects respiratory muscles and causes respiratory failure.

Toxic asphyxiants Cyanide, arsenic The mechanism of action of cyanide poisoning is reaction with the

trivalent iron of cytochrome oxidase in the mitochondria. Cellular respiration is thus inhibited, resulting in lactic acidosis and cytotoxic hypoxia

CHEMİCAL WEAPONS

Pulmonary irritants Fosgene, chlorine, ammonia Direct lung tissue injury resulting pulmonary edeme

Blistering agents Sulfur mustard Toxicity to the eyes, skin, and lungs occurs via direct

contact with the toxic substance

The main syndromes that suggest terrorist release of chemical weapons are neurologic, pulmonary, and skin and eye symptoms.

Leading cause of death due to fi res

Three injuries: thermal injury to the upper airways, chemical injury to the tracheobronchial tree, Systemic poisoning due to carbon monoxide and/or cyanide

SMOKE İNJURY

When a patient presents with known or suspected smoke inhalation, the patient’s airway, breathing, and circulation should be immediately assessed. If indicated, cardiopulmonary resuscitation should be performed

Intubation is justified if any of the following is present: stridor, use of accessory respiratory muscles, significant respiratory distress, hypoxemia, hypoventilation, deep burns to the face or neck, edema of the oropharynx.whereas close observation for 24 hours

Patients who do not require mechanical ventilation should receive supplemental oxygen using a fraction of inspired oxygen (FiO2) of 100 percent. An arterial blood gas should be sent for co-oximeter measurement of oxyhemoglobin saturation, carboxyhemoglobin concentration, and methemoglobin concentration.

Carbon monoxide (CO) poisoning should be presumed in any patient who presents following smoke inhalation until it is excluded by a normal carboxyhemoglobin level. 100% oxygen or hyperbaric oxygen treatment shoul be given

Pneumonia, ARDS, hypermetabolism, Reactive airway disease syndrome may occur lately

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