Acute Carbon Monoxide Poisoning in a Filipino Household: A Case Report

There are multiple reports already regarding acute carbon monoxide (CO) poisoning in the Philippines secondary to the misuse of portable generators, especially during times of typhoons. We present a case of unintentional carbon monoxide poisoning in a Filipino household wherein our index patient is among the five members who were unconscious before they were rushed to the hospital. Three of the household members, on the other hand, were found dead. The index patient had an increased serum fraction percentage of carboxyhemoglobin level and presented with rhabdomyolysis during admission. Neuroimaging confirmed a hypoxic-ischemic encephalopathy secondary to carbon monoxide intoxication. Even without hyperbaric oxygen therapy, the patient improved with adequate hydration, early rehabilitation, and trauma-focused psychotherapy.


Introduction
The Philippines' geographical location makes it highly susceptible to natural disasters, thereby producing numerous calamity-related damages and casualties [1].In times of post-typhoon power shortages, dieselpowered portable generators have been used by many in the far-flung provinces [2].However, the use of generators caused several accidental and unintentional carbon monoxide (CO) poisoning cases and deaths worldwide [3,4].These pieces of equipment emit carbon monoxide and, when placed in an enclosed space, could cause a buildup of CO [5] and ultimately wreak havoc on patients.
We now present a case report of acute carbon monoxide intoxication in a Filipino household due to a portable generator.We specifically highlighted an index patient who was fully worked up during his admission.

Case Presentation
A 34-year-old male was brought to the emergency room due to altered mental status.He was seen by neighbors lying unconscious, together with his wife, their three children, and three other housemates.Upon investigation by the medical team, it was found that the portable generator was placed inside their house, after experiencing a strong typhoon a day prior.Three family members were already dead, but the remaining unconscious members were brought to various hospitals for further management.Three of the members were brought to our emergency room, and the index patient was referred to different specialties, including the neurology service.Upon examination, the patient had normal vital signs and was hooked to 10 L per minute of oxygen via a face mask for oxygen support along with adequate hydration.The patient was encephalopathic and was seen drowsy with unsustained eye opening, with incomprehensible speech, and unable to follow commands.No lateralizing signs of weakness, numbness, or pathologic reflexes were seen.

TABLE 2: Serial blood examination during admission
Apart from the increased creatinine levels, the patient also presented with muscle tenderness and slightly darker urine output, to which the attending physicians entertained rhabdomyolysis.Table 3 shows increased urine red blood cell count and slight proteinuria.Moreover, muscle enzymes were also markedly elevated at first but had decreasing trends as aggressive hydration continued (shown in

TABLE 4: Muscle enzymes
Due to the unavailability of a pulse carbon monoxide oximetry, a serial determination of blood gas was employed (shown in Table 5).An increasing trend of fraction percentage of carboxyhemoglobin was seen but stabilized after the fourth hospital day.Apart from the carboxyhemoglobin level, the patient's metabolic acidosis also resolved eventually.During this time, the patient's neurological status improved significantly as he had sustained wakefulness with correct and consistent responses.He also underwent cranial magnetic resonance imaging (MRI) (seen in Figure 1), which showed restricted diffusion in the bilateral globus pallidus area on diffusion-weighted imaging (DWI) sequence with associated dropout signal in apparent diffusion coefficient (ADC) map.Moreover, there is a low signal intensity in the T1-weighted image with hyperintense signals on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images.On gradient echo (GRE) imaging, tiny foci of increased susceptibility are noted, which may represent microhemorrhages.All the findings represented changes seen in post-hypoxic encephalopathy, consistent with the patient's exposure to carbon monoxide.

FIGURE 1: MRI axial, cross-sectional view
A) Diffusion-weighted imaging (DWI), B) apparent diffusion coefficient (ADC) map, C) T1-weighted, D) T2weighted, E) T2 fluid-attenuated inversion recovery (FLAIR), and F) gradient echo (GRE) The red arrows pointing to lesions situated around the bilateral globus pallidus MRI: magnetic resonance imaging The patient was eventually started physical rehabilitation for a continuous and steady recovery.Moreover, he was referred to a psychiatry service for trauma-specialized psychotherapy.He was also started with an antidepressant prior to discharge.The two other family members admitted to our institution were also discharged well and stable.

Discussion
Carbon monoxide is a colorless, nonirritating gas, which is a byproduct of combustion.Fire-related smoke inhalation is responsible for the majority of CO poisoning cases.However, it is also seen in fuel-burning devices, gasoline-powered generators, and motor vehicles operating in poorly ventilated spaces [3,6].
As the carbon monoxide gets inhaled, it binds to the iron moiety of heme with significant affinity compared to oxygen.This then results in decreased oxygen delivery to tissues, leading to subsequent damage [7].A wide range of symptoms, from nonspecific constitutional symptoms such as headache, drowsiness, and fatigue to altered mental status leading to coma, can be seen.However, it all depends on the fraction inspired percentage of carbon monoxide, the patient's baseline comorbidities, and the duration of exposure to the toxin [8].
Studies have also demonstrated carbon monoxide intoxication producing delayed neurological sequelae (DNS), which appear around 2-40 days after a lucid interval post intoxication, followed by recurrent intermittent neuropsychiatric symptoms [6,9].The MRI findings of such showed lesions in the basal ganglia, white matter, or globus pallidus [9], which were present in our index patient.
Rhabdomyolysis as a complication of carbon monoxide poisoning has been reported in the literature.Muscle necrosis secondary to CO poisoning leads to the release of myoglobin from the skeletal muscle, which in turn causes acute kidney injury [10].Our patient had muscle tenderness with increased muscle enzymes.Adequate hydration was given along with continuous close surveillance reversing the initial acute kidney injury.
Hyperbaric oxygen therapy has been regarded as the initial therapy for acute carbon monoxide poisoning.However, this alone as a standard therapy is still unclear and remains controversial [6,7,9].Also, this therapy still has undetermined effects on the carbon monoxide-associated delayed neurological sequelae [9].

TABLE 1 : Complete blood count
Upon admission, the patient initially had signs of hepatic injury as evidenced by elevated liver enzymes.Moreover, he had an increasing trend of creatinine as high as 576.3 umol/L (shown in Table2), but this eventually decreased thereafter.

TABLE 3 :
Urinalysis RBC, red blood cell; WBC, white blood cell; HPF, high power field

TABLE 5 : Serial arterial blood gas determination pCO
2 , partial pressure of carbon dioxide; HCO 3 , bicarbonate; pO 2 , partial pressure of oxygen