Special Pulmonary Problems

1. Special PulmonaryProblems Prof. Sevda Özdoğan 2013

2. Drowning • Decompressionsickness, Barotrauma, Scubadiving • AcuteMountainsickness, highaltitudeproblems • Exposuretochemicalweapons • Smokeinjury

3. Drowning • Every year, drowning accounts for at least 500,000 deaths worldwide, Statistics for nonfatal drowning are more difficult to obtain, but nonfatal drowning events may occur several hundred times as frequently as reported drowning deaths • FatalDrowning: Deaththatoccurswithin 24 hours of submersion in a liquidmedium • NonfatalDrowning: Survival, at least temporarily, after suffocation by submersion in a liquid medium “Aprocess resulting in primary respiratory impairment from submersion or immersion in a liquid medium”

4. 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 efforts 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 affects every organ system, with the major component of morbidity and mortality being related to cerebral hypoxia

5. Formerly,the distinction between salt water and fresh water drowning wasemphasized: • 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 whichis unusual for nonfatal drowning victims to aspirate more than 3 to 4 mL/kg,

6. Results of bothtypes of drowning • Decreasedlung compliance, • Ventilation-perfusion mismatching, • Intrapulmonaryshunting, leading to hypoxemia • Diffuseorgan dysfunction • The temperature of the water and the presence of contaminants may affect patient outcomes

7. END ORGAN EFFECTS • Pulmonary • Hypoxemia • Washoutsulfactant (anoxicdegradation, inactivation) • Noncardiogenicpulmonaryedema • Aspiration of gastriccontent • ARDS • Neurological • Hypoxemianeuronaldamage • Cerebraledema • İncrease in intracranialpressure

8. Cardiovascular • Arrhythmias secondary to hypothermia and hypoxemia • Acidbaseandelectrolites • A metabolic and/or respiratory acidosis is often observed • Severe electrolitechangesrarelyduetoswallowedextremelyconcentratedseawater • Renal • Failure rarelydue to acute tubular necrosis resulting from hypoxemia, • Coagulaton • Hemolysis and coagulopathy are rare

9. management • Prehospitalcare • Ventilation (tworescuebreathing), resuscitation • Injurystabilization • Posturaldrainage techniques to remove water from the lungs are of no proven value • Oxygensupplementation • Rewarminghypothermicpatients • Arrhythmiasrequirenoimmediatetreatment • Emergencydepartmentcare • Frequentvital sign measurements and clinical reassessment • Immediateintubationif: • 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

10. supplementaloxygen • NIMV • Nasogastricdecompression • Glucosemeasurement • Traumaevaluation • Rewarming • Continueresustation (forseveralhours) in hypotermicpatients • Symptomaticpatients in goodconditionshould be monitorizeduntilthesymptomsandphysiologicdisturbancesresolve • Hospitalcare

11. Factorsthatcausepoorprognosis: • Duration of submersion >10 minutes • Time toeffectivebasic life support >10 minutes • Resuscitationduration >25 minutes • Watertemperature >10ºC (50ºF) • Age <3 years • Glasgow comascale <5 (comatose) • Persistentapneaandrequirement of cardiopulmonaryresuscitation in theemergencydepartment • ArterialbloodpH <7.1 uponpresentation

14. Decompressionsickness, Barotrauma, Scubadiving • Emergenciesspecifictodiving: • Barotrauma, includingarterialairembolism • Decompressionsickness • Nitrogennarcosis • Twobasic 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.

15. barotrauma • 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.

16. Pulmonarybarotrauma • 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

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

19. pneumothorax • Spontaneouspneumotorax is rare (10%) • Historyof spontaneous pneumothorax, bullae, or cystic lung disease increasethe risk • If this occurs at a significant depth, the pleural gas expands as the diver ascends and can result in a tension pneumothorax • dyspnea, • chestpain, • tachycardia, • hypotension, • cyanosis, • distendedneckveins, • hyperresonancetopercussion, • unilateraldecrease in breathsounds, • Accompanyingsubcutaneousemphysema(25%)

20. Arterialgasembolism • 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

21. After reaching the systemic arterial circulation, gas emboli typically break up andproduce 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

22. dysrhythmias, myocardial infarction, and/or cardiac arrest • Focalmotor, sensory, or visual deficits to seizures, loss of consciousness, apnea, and death. • Cyanoticmarbling 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.

23. Earbarotrauma: 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 filling with serous fluid or blood or to inward rupture of the tympanic membrane • Sinusbarotrauma • Dentalbarotrauma

24. DECOMPRESSION SICKNESS • 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 inflammatory cascades.

25. 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

26. symptoms • Mild form: • Localisedjointpain • Skin pruritus, localisederythema, cyanosis • Lymphatic obstruction by bubbles, although rare, can lead to pain, lymphadenopathy, and localized edema • Severe decompression: • Nervoussysteminvolvement: damagetothespinalcord • Paresthesia, weakness, paraplegia, loss of syphinctercontrol • Pulmonaryinvolvement: • wheezing, dyspnea, and pharyngeal irritation • Right hearthfailure, circulationcollapse, death

27. treatment • Hydration • Administrationof 100 percent oxygen, • Positioningthe patient in the left lateral decubitus and mild Trendelenburg (bed angled downward toward head) position in an effort to restore forward blood flow • Hyperbaricoxygentherapy Complete resolution of thesymptoms is seen in 75% even in the severe form ifthetreatmentifstartedimmediately

28. Nitrogennarcosis • 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.

29. AcuteMountainsickness • High altitudeillness: 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 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.

30. The first 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.

31. 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 altitudepulmonaryedemaoccurs • Cerebralbloodflowincreases in responsetohypoxemiathatcauseheadacheandhighaltitudecerebraledema • Periodicbreating at nonREMsleepoccursduetohypoxemiaandhypocapnia

32. Symptoms of AMS • Headache • Fatigue • Lightheadedness • Anorexia • Nausea • Vomiting • disturbed sleep with frequent awakening • mild shortness of breath with exertion. Symptoms may be mild or severely debilitating.

34.  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

35. Treatment • AcuteMountainSickness • Treatment of AMS is based upon symptom severity and, in mild cases, patient preference • Supplemental oxygen • Avoidfurtherascend • Limit physicalactivity • Avoidalcoholseg • Basic analgesicsforheadacheandantiemetics • Occasionalydescent • Acetozolamideincreasetheacclimatization • Dexamethazone

36. High altitudecerebraledema • Descent is the definitive treatment. • Dexamethasone • supplemental oxygen, • hyperbaric therapy • Gradualascent should be emphasized

37. Chemicalweapons • 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. • Toxicasphyxiants • 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

38. Pulmonary irritants • Fosgene, chlorine, ammonia • Direct lungtissueinjuryresultingpulmonary edeme • Blisteringagents • Sulfurmustard • 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.

39. Smokeinjury • Leadingcause of deathduetofires • Three injuries: • thermal injury to the upper airways, • chemical injury to the tracheobronchial tree, • Systemicpoisoning due to carbon monoxide and/or cyanide

40. 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 justifiedifany of thefollowing 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

41. 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 carboxyhemoglobinlevel. 100% oxygenorhyperbaricoxygentreatmentshoul be given • Pneumonia, ARDS, hypermetabolism, Reactiveairwaydiseasesyndromemayoccurlately

42. Thankyou