Noncardiogenic Pulmonary Edema Associated with Accidental Hypothermia

Noncardiogenic Pulmonary Edema Associated with Accidental Hypothermia

sarcomas following radiation therapy alone (without chemotherapy) for a variety of tumors, clearcut epidemiologic data are lacking. T h e case present...

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sarcomas following radiation therapy alone (without chemotherapy) for a variety of tumors, clearcut epidemiologic data are lacking. T h e case presented herein represents the simultaneous occurrence of two separate neoplasms in which ionizing radiation, from multiple fluoroscopic examinations, may b e implicated as a causative factor. The physician must be aware of conditions for which ionizing radiation may have been used, either as part of the treatment itself or to evaluate the patient's condition during treatment. Such conditions include, among others, ankylosing spondylitis, tinea capitis, thymic enlargment,13spinal tuberculosis, tonsil or adenoid enlargement, acne, postpartum mas ti ti^,^^.^^ and infertility.

REFERENCES

1 Alexander J. The collapse therapy of pulmonary tuberculosis. Springfield, Ill: Charles C Thomas, 1937 2 Mann T. The magic mountain. New York: Vintage Books Edition, 1969:217 3 Boice JD, Monson R. Breast cancer in women after repeated fluoroscopic examinations of the chest. J Natl Cancer Inst 1977; 59:823-32 4 Boice JD. Multiple chest fluoroscopies and the risk of breast cancer. Read before the 12th International Cancer Congress, Oct 5-11, Buenos Aires, Argentina, 1978 5 Hmbec 2,Boice JD, Monson RR, Rosenstein M. Breast cancer after multiple chest fluoroscopies: second follow-up of Massachusetts women with tuberculosis. Cancer Res 1989; 49:229-34 6 Myrden JA, Hilk JE. Breast cancer following multiple fluoroscopies during artificial pneumothorax treatment of pulmonary tuberculosis. Can Med Assoc J 1969; 100:1032-34 7 Cook DC, Dent 0 , Hewitt D. Breast cancer following multiple chest fluoroscopy: the Ontario experience. Can Med Assoc J 1974; 111:406-10 8 Mays CW, Lloyd RD. Bone sarcoma incidence versus alpha particle dose. In: Stove BJ, Lee WSS, eds. Radiology of plutonium. Salt Lake City: JW Press, 1972 9 Baverstock KF, Papworth D, Vennart J. Risks of radiation at low dose rates. Lancet 1981; 1:430-33 10 Stebbings JH, Lucas H, Stehney A. Mortality from cancers of major sites in female radium dial workers. Am J Ind Med 1984; 5:435-59 11 Smith PG, Doll R. Late effects of X irradiation in patients treated for metropathiahaemorrhagica. Br J Radio1 1976;4922432 12 Meadows AT, DD'AngioGJ, Mike Y Banfi A, Hanis C, Jenkin RDT, et al. Patterns of second malignant neoplasms in children. Cancer 1977; 40:1903-11 13 Hildreth N, Shore R, Hempelmann L. Risk of breast cancer among women receiving radiation treatment in infancy for thymic enlargement. Lancet 1983; 2:273 14 Dvoretsky PM, Woodward E, Bonfiglio T, Hempelmann L, Morse I. The pathology of breast cancer in women irradiated for acute postpartum mastitis. Cancer 1980; 46:2257-62 15 Mettler FA, Hempelmann L, Dutton A, Pifer J, Toyooka E, Ames W. Breast neoplasms in women treated with x-rays for acute postpartum mastitis: a pilot study. J Natl Cancer Inst 1969; 43:803-11

Noncardiogenic Pulmonary Edema Associated with Accidental Hypothermia* Carlos E Morales, Maj, USAB MC; and RatrickJ ShoUo, Maj, USAB MC, EC.C.E

T h e pulmonary system may be significantly affected by hypothermia. T h e association between NCPE and hypothermia is controversial. A 59-year-old man with mild hypothermia presented with NCPE after passive external rewarming following accidental immersion in water. T h e patient's course was uneventful after 48 h, allowing immediate withdrawal of assisted ventilation and supplemental oxygen. (Chest1993; 103:971-73) FIo, = inspired oxygen concenh-ation; NCPE =noncardiogenic ulmonary edema; P(A-a)O, = alveolar-arterial oxygen pressure herence

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ypothermia appears to have a small effect on pulmonary mechanics and gas exchange. As compared to euthermic patients, lung volumes, airway resistance, compliance and P(A-a)O, disclose no signficant differences1-' Blunting of the ventilatory response to an increase in carbon dioxide tension has been described,= although the hypoxic drive appears to be unaffected.3 The development of NCPE related to hypothermia is controver~ial.~ A previous case report associated with severe hypothermia has been described.=The following case is one of NCPE associated with mild hypothermia in the setting of accidental water immersion.

CASEREPORT A 54year-old man was admitted to the medical intensive care unit with a diagnosis of acute respiratory failure after stabilization in the emergency department. This occurred during the month of April; local temperature was 66' F. The patient was caught in his automobile by flooding waters and had experienced accidental water immersion for 2 h. To avoid drowning, a nearby tree was used as support allowing unrestricted water flow below the level of his chest. Upon rescue, the patient was alert, oriented and denied aspiration of water. Initial pulse was regular at 130 beats per minute; blood pressure, 150/90 mm Hg; respiratory rate, 28 breaths per minute; and rectal temperature, 34OC measured by a low-reading thermometer. He complained of being cold and his physical examination disclosed a shivering patient with cold, pale skin that was othewise normal. At the time of admission, the hematocrit level was 43.9 and the white blood cell count was 2 0 , W c u mm with 88 percent neutrophils, 8 percent lymphocytes and 4 percent monocytes. The platelet count was 300,00O/cu mm. The serum electrolytes, creatinine and blood urea nitrogen values were within normal limits. The serum creatinine b a s e was elevated to 446 IUL, with normal MB bands; serum amylase was 141 IUL; serum albumin was normal; and the blood alcohol level did not r e d any alcohol being present. The urinalysis was normal. An electrocardiogram showed sinus tachycardia at a rate of 106 beawmin without J-point elevation. The chest roentgenogram on arrival at the hospital was *From the Department of Critical Care and Pulmonary Medicine, Wilford Hall USAF Medical Center, San Antonio, Tex. The opinions expressed herein represent those of the authors and not necessaril those of the United States Air Force or the Department o r ~ e f e n s e . CHEST 1 103 1 3 1 MARCH. 1993

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(Fig 2) and he was successfully extubated with an uneventful outcome.

FICUM 1. Chest x-ray film 4 h after presentation demonstrating diffuse bilatelal infiltrate.

normal. After passive external rewarming with warm (nonelectric) blankets and room temperature normal saline administered intravenously at a rate of 125 mlh (500 ml total) his rectal temperature mse to 3PC in 4 h. At this point, the patient complained of dyspnea and his respiratory rate was Wmin and his blood pressure was W 60 mm Hg with a pulse of 110 beats per minute. The patient remained alert and oriented with a normal neurologic examination. Pulse oximetry revealed oxyhemoglobin saturations below 90 percent despite the use of a non-rebreathing face mask with FIo* of 1.0. The uncorrected arterial blood gases after omtracheal intubation and assisted ventilation using a FIo of 1.0 were as follows: pH, 7.35; Pco,, 35 mm Hg; Po,, 345 mm Hg; saturation, 99.9 percent; and P(A-a)O,, 316 mm Hg.A repeat chest roentgenogram revealed a diffuse alveolar infiltrate without cardiomegaly, pleural effusion or an increase in the vascular pedicle width (Fig 1). To better define the patient's hemodynamic status, right heart catheterization revealed normal right atrial pressure of 6 mm Hg, pulmonary arterial wedge pressure of 12 mm Hg and cardiac index of 3.4 Wmin. Blood cultures were negative at 48 h. No empiric antibioticswere given. After 48 h his gas exchange normalized, the patient's chest roentgenogram was remarkable for clearingof the alveolar infiltrates

FIGURE 2. Chest x-ray film 48 h after presentation demonstrating resolution of ditfuse bilateral infiltrates

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Noncardiogenic pulmonary edema is a syndrome c h a m terized by pulmonary edema arising from increased lung microvascular permeability. Although a multiplicity of clinical states can lead to NCPE, the association with hypothermia andlor rewarming has been controversial." Adequate documentation in the literature of this association is lacking. Bloch,' using a surface cooling technique, subjected 25 conscious patients with cerebral astrocytoma to irradiation under prolonged whole-body hypothermia. Body temperature (rectal) was regulated to a selected mean temperature of 30"to 31°C. During rewarming, signs of pulmonary edema developed, which was associated with "drowsiness" and an increase in CSF pressure in the range of 295 to 370 mm. Relief of the pressure by removal of CSF correlated with resolution of dgns of pulmonary edema. On the basis of this observation, the author concluded that raising CSF pressure during rewarming could cause neurogenic pulmonary edema. O'Keeffd described a case of NCPE in the setting of severe hypothermia (27.0°C). As opposed to our patient, active external rewarming with a "K-thermia blanket" was used, and a rapid improvement of arterial oxygenation occurred upon rewarming in 3 h to a core temperature of 37.0°C. Unique to our case is the development of NCPE associated with a relatively mild degree of hypothermia after passive external rewarming. In two recent large serie+* involving a total of 530 patients with hypothermia, no case of NCPE was described. No other cases of NCPE have been observed by D. F. Danzl (communication, [written] February 1992). -Pulmonary complications associated with hypothermia are diverse. Chest congestion, due to impaired ciliary activity, may result in frothy sputum production and bronchorrhea resembling pulmonary edema." Pneumonia, depression of cough with atelectasis or aspiration or both the latter also have been described.ll ~ u r isevere i ~ hypothermia, retention of carbon dioxide and respiratory acidosis suggest an altered response to normothermic respiratory stimuli.1° The development of hypoxemia and pulmonary infiltrates may be related to one of these proposed mechanisms, in addition to a central mechanism as suggested by B1och.l Our patient experienced NCPE after passive external rewarming that resolved after 48 h of support with mechanical ventilation. Active external rewarming during experimental and clinical conditions may produce peripheral vasodilatation, hypotension and core temperature afterdrop.I0 Hemodynamic measurements were undertaken to exclude sudden central return of blood pooled in the extremities due to a depressed cardiovascu& system. The exact cause of the NCPE in the patient was unknown, although a central mechanism seems possible due to the fact that the patient had no evidence of pneumonia, aspiration, macroatelectasis or bronchorrhea on presentation to the emergency department. 1 Hedley-White J, Pontoppidan H. Laver MB, Hallowell P, Ben-

dixen HH. Arterial oxygenation during hypothermia. Anesthesiology 1965; 26:595-603 2 Blair E, Esmond WC. Atlas S, Cowley RA. The effect of hypothermia on lung function. Ann Surg 1964; 160:814-23 3 Hardy JD, Bard P. Body temperature regulation. In: Mountcastle VB. ed. Medical physiology. St. Louis: CV Mosby, 1974: 1305 4 Rosenkld JB. Acid-base and electrolyte disturbances in hypothermia. Am J Cardiol 1963; 12:678-82 5 Ferguson J, Eptein F, Van De Leur J. Accidental hypothermia. Emerg Med Clin North Am 1983; 1:619-37 6 O'Keefe KM. Noncardiogenic pulmonary edema from d d e n tal hypothermia. Colorado Med 1980; 77:106-07 7 Bloch M. Cerebral effects of rewarming foUowing prolonged hypothermia: significancefor the management ofsevere craniocerebral injury and acute pyrexia. Brain 1967; 90:769-84 8 Danzl DF, Pozos RS. Multicenter hypothermic survey. Ann Emerg Med 1987; 16:1042-55 9 White JD. Hypohernia: the BeUevue Experience. Ann Emerg Med 1982; 11:417-24 10 Danzl DF. Raos RS, Hamlet MI? Accidental hypothermia. In: Auerbacb PS. Geehr EC, eds. Management of wilderness and environmentalemergencies. St. Louis: CV Mosby, 1989: 35-76 11 Fikgerald FI:Jessop C. Accidental hypothermia: a report of 22 cases and review ofthe literature. Adv Intern Med 1982;27:12750

High-Altitude Pulmonary Edema in Partial Anomalous Pulmonary Venous Connection of Drainage wlth Intact Atrial Septum* Anito Derk M.D.;t and Frank H. Bosch. M.D.$

Partial anomalous pulmonary venous drainage may be the c a w of h-mh and averperfusion of the lungs and then-efban important b t o r in the pathogenesis of highaltitude pulmonary edema ( W E ) .

(c-

1993; 103:913-74)

igh altitude pulmonary edema been H entity since Its underlying pathophysiology remains unclear. The occurrence of partial recognized

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(HAPE) has

FIGURE 1. Chest x-ray film showing HAPE. and a nonproductive cough. He descended to 2,400 m and was taken to a hospital. On admission, he was cyanotic. The blood pressure was 15Q1100 mm Hg, and the pulse was 90 beats per minute. Rales were present over both lung bases. A grade 3/6 midlate systolic crescendo-decrescendo murmur and an accentuated pulmonary second sound were heard along the left sternal border. Blood gas analysis showed respiratory alkalosis. An x-ray film of the chest revealed pulmonary edema, especially in the leR lower lobe, and prominent dilated main pulmonary arteries (Fig 1). The ECG showed sinus rhythm with signs of right atrial enlargement. The patient was treated with nifedipine (20 mg). Because an ASD or an anomalous pulmonary venous return was considered, further examination was performed. On the bicycle ergometer a significant decrease in partial oxygen pressure was measured: 93 mm Hg to 77 mm Hg. Cardiac catheterization showed an intact ahid septum but anomalous drainage of the upper and middle lobe vein of the right lung into the superior vena cava at the junction

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anomalous pulmonary venous drainage (PAPVD) without an associated atrial septa1 defect (ASD) is uncommon. We describe one patient with PAPVD who experienced two episodes of HAPE at moderate altitude. The question is if the hemodynamic alterations in this cardiac abnormality play a role in the pathogenesis of HAPE. A Byearold mountaineer living in Holland has been climbing regularly in mountains of3.000 to 7.000 m for 12years. In December 1989. he made a hip to the Swiss mountains. In three days, he ascended to 3,800 m. At night, he developed shortness of breath Academic Medical Center, *From the Department of Cardio hsterdam, and the Department91nterd Medicine, ~ j Hospital, Amhem, the Netherlands. ?Department of C a r d i o h . $De+ent of Internal Medicine.

showing anomalous venous ~ FIGURE ~ 2. Cardiac m ~ drainage of right upper and middle lobe vein into right atrium (RA) and of right lower lobe vein into left atrium (LA). WD. Pulmonary vein dexter. CHEST 1 103 1 3 1 MARCH. 1993

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