Continuous Renal Replacement Therapy in the Treatment of Severe Acute Mountain Sickness

Abstract

Acute mountain sickness (AMS) is usually seen in unacclimatized individuals ascending to a high altitude within a short period of time. Severe cases may be complicated with multiorgan dysfunction syndrome (MODS), which results in very high mortality. We reported a case of a 20-year-old girl who developed AMS complicated with high altitude pulmonary edema (HAPE), high altitude cerebral edema (HACE), and acute renal failure. Continuous renal replacement therapy (CRRT) was successfully carried out in this patient and achieved satisfactory effects. The treatment of this patient suggests that early intervention of CRRT may be a useful therapy for patient with severe AMS, especially those with MODS.

Keywords:

• CRRT
• acute mountain sickness

Acute mountain sickness occurs when unacclimatized individuals ascend to high altitude within a short period of time. In severe cases, patients may have high altitude pulmonary edema (HAPE) or high altitude cerebral edema (HACE) and even multiorgan dysfunction syndrome (MODS), which is related with a considerably high mortality rate.[1–3] The effects of conventional treatments were poor in severe cases. Continuous renal replacement therapy (CRRT) can be used to steadily remove fluid and maintain homeostasis.[4] In this paper, we presented a case of severe AMS successfully treated by CRRT.

CASE REPORT

A 20-year-old previously healthy female traveled from Chengdu, China (altitude 540 m) to Mt. Minya Konka (altitude >5500 m) in a one-day bus travel. Soon after arriving, she felt a headache at bilateral occipital region, along with dizziness, nausea, dyspnea and frequent vomiting. Oxygen therapy and antiemetics (metoclopramide) were administrated in local hospital (two days ago); however, no relief was observed: she still complained about persistent headache, intermittent vomiting, and decreased urine output (<200 mL/d). One day later, she was transferred to a hospital at 600 m, but oxygen, dexamethasone, furosemide, and analgesic (aspirin) did not relieve the symptoms. Four hours later, the patient felt severe pain at bilateral temporal areas accompanied by vertigo and projectile vomiting, which was followed by several instances of systemic convulsion along with loss of consciousness. Therefore, she was sent to the Emergency Department of our hospital.

Physical examination indicated the following data: T 37°C, HR 145 bpm, R 45 time/min, BP 175/105 mmHg, restlessness, light coma status, no response to sound stimulus, Glasgow score of 6; equal bilateral pupils (diameter = 4 mm), weakened light reflex, meningeal irritation sign (−), pathologic reflex (−); normal heart and abdominal examination; diffused loud rales and crackles (as indicated by pulmonary auscultation), and moderate edema of lower limbs. Cranial CT scan indicated diffused cerebral edema. Lab test indicated serum creatinine, 1838 umol/L; BUN, 38.8 mmol/L; UA, 916 umol/L; Na, 125 mmol/L; K, 5.9 mmol/L; SaO₂, 85%; WBC, 1.1×10⁹/L; neutrophil, 82%; platelet, 221×10⁹/L; and hemoglobin, 120 g/L. The patient was diagnosed with acute severe mountain sickness, complicated with acute cerebral edema, acute pulmonary edema, and acute renal failure. The APACH II score was 31. Furosemide (40 mg iv), lanatoside C (0.4 mg iv), nitroglycerol (2–4 mg/hr ivgtt), glycerol/fructose (250 ml ivgtt), face mask oxygen therapy, and other symptomatic treatments were applied. However, convulsions continued, and conscious disturbance deteriorated. Arterial blood gas analysis revealed that SaO₂ and PaO₂ of the patients were decreasing progressively. Therefore, tracheal intubation and mechanical ventilation were performed immediately.

In order to treat the acute pulmonary edema as well as acute renal failure, continuous blood purification was applied. Continuous veno-venous hemofiltration was applied using Diapact CRRT machine (B. Braun) and Fresenius AV 600 hemofilter (1.4m²). 3,000 mL/h replacement fluid was given by pre-dilution. Low molecular weight heparin was used as anticoagulant. Blood flow rate was set as 250 mL/min. Ultrafiltration was set as 650 mL/h at the beginning. During the CRRT treatment, patients' vital signs gradually stabilized (HR and BP decreased). Two hours later, HR reduced to 125 bpm, and BP decreased to 147/86 mmHg. Convulsion stopped along with the improvement of conscious status. Six hours later, pulmonary auscultation indicated remarkable decrease of rales and moist bubbles. We then decreased the ultrafiltration rate to 200 mL/h. After 48 hours of continuous CVVH treatment, mechanical ventilation was stopped, and APACHE II score was 22. Patient's conscious was recovered and she responded to sound stimulus (Glasgow score 10). Urine output increased to 700 mL/24h. Lab test indicated significantly recovery of renal function (Scr 558 umol/L, BUN 14.2 mmol/L). Therefore, we decreased the ultrafiltration rate to 100 mL/h. After 72 hours of CVVH treatment, the patient regained consciousness (Glasgow score 15). Urine output increased to 930 mL/d. Patient's renal function improved gradually (Scr 245 umol/L, BUN 8.6 mmol/L). Hence, CVVH treatment was stopped, and her APACHE II score was 12. Seven days later, the patient was discharged from the hospital with completely restored renal function (urine output 2000–3000 mL/24h, Scr 112 umol/L, BUN 7.5 mmol/L). The patient was followed up for more than two years; the heart, pulmonary, and kidney functions remained normal during the follow-up.

DISCUSSION

Acute mountain sickness (AMS) is a common cause of morbidity and mortality in unacclimatized people shortly after ascent to high altitude (>3000 m). Usually, AMS is a syndrome of nonspecific symptoms such as gastrointestinal symptoms like anorexia, nausea or vomiting; insomnia; dizziness; headache; and lassitude or fatigue. In severe cases, patients may have high altitude pulmonary edema (HAPE) or high altitude cerebral edema (HACE) and even multiorgan dysfunction syndrome (MODS).[1]

The actual pathophysiologic mechanism that causes AMS is unknown. Hypoxia at high altitude may be the major factor.[[1] Hypoxia causes hypoxemia and induces neuroendocrinologic and hemodynamic changes in cerebral and pulmonary circulation. These changes lead to pulmonary and cerebral blood overflow and an increase in capillary pressure and vascular permeability, and finally cause fluid leakage, which results in cerebral edema and pulmonary edema.[1–3],[5],[6] Several studies indicated that patients with AMS, especially those who didn't receive proper treatment, are likely to be complicated with acute renal failure (ARF).[7],[8] It is suspected that hypoxemia may cause cardiac output decrease and renal artery constriction, which results in hypoinfusion of kidney and leads to ischemic kidney injury. Meanwhile, persistent vomiting often causes hypovolemia in patients with severe AMS, which may lead to pre-renal ARF.[9] Moreover, the administration of certain medicines, especially high doses of mannitol and NSAIDs, may make the situation worse.

The treatment of AMS includes descent to a low altitude area, oxygen therapy, and medications such as acetazolamide, dexamethasone, nifedipine, NSAIDs, diuretics, and dehydrator (mannitol or glycerol + fructose).[1] However, in severe cases (especially those complicated with ARF), mortality rate is considerably high despite these treatment. In this case, the patient developed severe AMS complicated with MODS (HAPE, HACE, ARF).[1],[6] HAPE aggravates the degree of hypoxemia and causes ischemic injury to the brain and kidney, which leads to HACE and ARF. ARF causes water and sodium retention, electrolytes disorder, and acidosis, which in turn aggravates HAPE and HACE. Therefore, a vicious cycle of pathophysiologic change was established, which makes the clinical treatment very difficult and even ineffective.

Continuous blood purification is a newly developed method of renal replacement therapy; it can remove water, waste, and even inflammatory factors slowly and steadily. It is widely used in patients with critical situations. It has already been reported that CRRT could improve the survival of patient with ARF, ARDS, SIRS, and MODS.[10]

In this patient, conventional therapeutic measurements were contradictory to each other: on the one hand, treatment of HACE needs dehydrate agents such as mannitol, while on the other hand, mannitol is contraindicated in oliguric ARF. Meanwhile, the volume control of the patient is very difficult: on the one hand, continuous vomiting caused severe loss of fluid volume, which leads to the pre-renal ARF and required fluid infusion; on the other hand, acute pulmonary edema indicated the volume overload of the lung, which demands rapid removal of volume load. Therefore, a dilemma was met during the treatment. Regarding all of the difficulties met in the treatment, in order to control HACE and HAPE, balance fluid load, eliminate metabolic waste, maintain homeostasis, and remove inflammatory factors, CRRT treatment was indicated. CVVH treatment reduced the volume load of the patient steadily in a well-controlled manner, which reversed HACE and HAPE status. Patient's conscious status improved progressively and recovered from coma 24 hours after CVVH treatment. Meanwhile, the patient's respiratory function improved, and the strength of respiratory support (FiO₂, respiratory rate, PEEP support) needed decreased after CRRT treatment. When the HAPE and HACE were relieved, we decreased the ultrafiltration rate, which helps to maintain a sufficient renal infusion. With the reversion of hypoxemia and maintenance of appropriate volume load after CVVH treatment, renal hypoinfusion status was reversed and ischemic injury of kidney was removed. After seven days of CRRT treatment, the patient's HACE, HAPE, and ARF were effectively reversed, and the patient was cured without sequela.

In this case, CRRT is actually the only practicable treatment that could help the patient. It is reported several AMS patients are complicated by renal failure[7],[8]; we think applying CRRT may shed some light on the treatment of these patients and may be helpful in reducing the mortality of patients.

CONCLUSION

Early intervention of CRRT may be a useful therapy for patient with severe AMS, especially those with HACE or HAPE complicated with ARF.

DECLARATION OF INTEREST

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.