Authors: Lauren Robertson (Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio, USA), Haley Coughlin (Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio, USA), Jiwoong Her (Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio, USA; Department of Clinical Sciences, North Carolina State University College of Veterinary Medicine, Raleigh, North Carolina, USA)
Categories: Case Series, canine, carbon monoxide, carboxyhemoglobin, high‐flow nasal cannula oxygen therapy, smoke inhalation
Source: Journal of Veterinary Emergency and Critical Care
Doi: 10.1111/vec.70083
Authors: Lauren Robertson, Haley Coughlin, Jiwoong Her
To report the use of high‐flow nasal cannula oxygen therapy (HFNOT) in three dogs with carbon monoxide poisoning resulting from smoke inhalation.
Three dogs were presented to the emergency room with carbon monoxide poisoning associated with house fires. Blood CO‐oximetry at the time of presentation confirmed markedly increased carboxyhemoglobin levels. The dogs were treated with 4–7 h of HFNOT to eliminate carboxyhemoglobin. The calculated half‐lives of carboxyhemoglobin during HFNOT for Dogs 1, 2, and 3 were 79, 86, and 77 min, respectively. All three dogs survived to discharge, and no delayed complications of carbon monoxide poisoning were reported.
To the authors’ knowledge, this is the first case series of dogs treated with HFNOT for carbon monoxide poisoning. HFNOT was shown to be effective at removing carbon monoxide, reducing the half‐life of carboxyhemoglobin from 77 to 86 min. The half‐life of carboxyhemoglobin and the effectiveness of HFNOT should be further investigated in a larger sample of dogs.
Carbon monoxide (CO) poisoning in companion animals is often associated with house or structural fires [1]. CO competes with oxygen for binding to hemoglobin (Hb), reducing its oxygen‐carrying capacity [2]. CO binding to Hb also increases the affinity for oxygen to Hb, shifting the oxygen–Hb dissociation curve to the left and further decreasing oxygen delivery to tissues. Clinical signs of CO poisoning in dogs include nausea and vomiting, tachypnea, hypothermia, altered mental status, seizures, coma, and death [1, 3, 4, 5, 6]. Oxygen therapy is the mainstay of treatment for CO poisoning, decreasing the elimination half‐life of carboxyhemoglobin (COHb) by competitive inhibition. The American College of Emergency Physicians recommends timely initiation of normobaric oxygen therapy or hyperbaric oxygen therapy [7].
High‐flow nasal cannula oxygen therapy (HFNOT) delivers warmed and humidified oxygen with a high flow rate up to 60–70 L/min and an FiO2 ranging from 0.21 to 1.0 [8]. Compared with conventional oxygen therapy (COT), HFNOT delivers a higher FiO2 while providing physiological advantages, such as improved humidification and gas exchange [8]. In the human literature, HFNOT was more effective in reducing the half‐life of COHb in patients with CO poisoning compared with other conventional normobaric oxygen therapies [9, 10, 11, 12]. To the authors’ knowledge, there has only been one case report describing the use of HFNOT in a dog with CO poisoning [3]. The current case series highlights the use of HFNOT in three dogs suffering from smoke inhalation and subsequent CO poisoning.
A 7‐year‐old intact female Boxer weighing 27.0 kg was presented to the Ohio State University Veterinary Medical Center (OSU‐VMC) by the fire department for smoke inhalation from a house fire. Before presentation, supplemental flow‐by oxygen had been administered via face mask.
Upon presentation, the patient had increased respiratory effort and a soft cough. An examination revealed harsh bronchovesicular sounds bilaterally, tachycardia (heart rate 160/min) with occasional premature beats, and brick‐red mucous membranes. Venous CO‐oximetry1 was performed, revealing increased levels of COHb (21.8%; reference interval [RI]: 1.3–2.7 [13]) and PvCO2 (53.5 mm Hg; RI: 32.6–48.3). Methemoglobin (MetHb) levels remained within normal limits (0.4%; RI: 0.1–0.4 [13]). Initial stabilization of the patient consisted of a crystalloid fluid bolus2 (10 mL/kg, IV, over 30 min), flow‐by oxygen supplementation, and sedation consisting of butorphanol3 (0.2 mg/kg, IV), acepromazine4 (0.02 mg/kg, IV), and dexmedetomidine5 (1 µg/kg, IV).
Given evidence of moderate [14] CO poisoning, HFNOT was initiated within 1 h of presentation using a veterinary HFNOT system6 at 1 L/kg/min, an FiO2 of 1.0, and a temperature of 35°C. After 5 h, CO‐oximetry showed markedly improved COHb levels (2.1%; RI: 1.3–2.7) and normal oxyhemoglobin (O2Hb 97.0%; RI: 94–99). The patient had developed mildly increased respiratory effort before CO‐oximetry was rechecked; therefore, given the normal O2Hb, a gradual de‐escalation from HFNOT was attempted. The patient became acutely dyspneic within an hour of decreasing the FiO2, and HFNOT parameters were increased from a flow rate of 1 to 1.5 L/kg/min and from an FiO2 of 0.8–1.0.
On Day 2 of hospitalization, an arterial blood gas1 analysis showed a PaO2/FiO2 ratio of 112, with a PaO2 of 111.7 mm Hg at an FiO2 of 1.0, which was concerning for the development of noncardiogenic pulmonary edema (NCPE) from smoke inhalation, thermal injury, or acute respiratory distress syndrome (ARDS). Additionally, there was evidence of upper respiratory thermal injury with gingival ulcerations, stertor, and mucoid nasal discharge. After 20 h of HFNOT, the patient was weaned to an oxygen cage with an FiO2 of 0.4 with pulse oximetry (SpO2) monitoring, where the SpO2 remained above 94%. Oxygen therapy was discontinued on Day 4. The next day, the patient developed increased expiratory effort and an SpO2 of 91%, possibly due to lower airway obstruction or bronchospasm from shedding mucosal casts, progressive NCPE, or secondary pneumonia, although this was not confirmed with thoracic imaging. The patient was provided traditional nasal cannula oxygen therapy at a rate of 93 mL/kg/min for 13 h. A repeat arterial blood gas1 analysis obtained before discontinuing conventional nasal cannula oxygen therapy showed overall improvement, with PaO2 of 75.5 mm Hg on FiO2 of 0.21, for a PaO2/FiO2 ratio of 359. Oxygen therapy was successfully discontinued on Day 5, and after 6 days of hospitalization, the patient was discharged with oral sedatives, a nonsteroidal anti‐inflammatory pain medication, and topical treatment for bilateral superficial corneal ulcers.
A 2‐year‐old neutered female American Staffordshire Terrier weighing 26.5 kg was presented to the OSU‐VMC by the fire department for smoke inhalation from a house fire. In transit to the hospital, the patient had received supplemental flow‐by oxygen via face mask and midazolam7 (0.09 mg/kg, IM).
Upon presentation, the patient was quiet with an increased heart rate (160/min) and rapid capillary refill time. Doppler blood pressure was mildly decreased at 80 mm Hg but increased to 140 mm Hg with a crystalloid fluid bolus2 (10 mL/kg, IV, over 20 min). A harsh cough and stertorous breathing were appreciated, although the patient was eupneic with no changes in bronchovesicular sounds. A neurological assessment revealed a mild proprioceptive ataxia without any other deficits appreciated.
Arterial CO‐oximetry1 and blood gas analysis were performed, revealing an increased COHb at 29.6% (RI: 1.3–2.7), decreased O2Hb at 69.9% (RI: 94.0–98.0), normal PaO2 of 109 mm Hg, and normal MetHb at 0.4% (RI: 0.3–1.5). Given evidence of moderate [14] CO poisoning, the patient received butorphanol3 for sedation (0.2 mg/kg, IV), and HFNOT was initiated within 30 min of presentation using a veterinary HFNOT system6 at 1 L/kg/min, an FiO2 of 1.0, and a temperature of 37°C. The flow rate was decreased to 0.6 L/kg/min after 2 h due to the patient's intolerance of the higher flow rate. After 7 h, a repeat arterial CO‐oximetry and blood gas1 analysis showed normalized COHb at 0.5% (RI: 1.3–2.7) and O2Hb at 98.5% (RI: 94.0–98.0), as well as an increased PaO2 at 499 mm Hg. HFNOT was discontinued at this time.
On Day 2 of hospitalization, the patient's ataxia had resolved. The patient was eupneic on room air with a persistent, harsh cough. Point‐of‐care ultrasound revealed occasional B‐lines bilaterally. Analgesia was added due to perceived airway discomfort (methadone8, 0.1–0.2 mg/kg, IV, q 4–8 h). After an additional 24 h of monitoring, the patient remained eupneic and became comfortable without analgesia. On Day 3, the patient was discharged with oral sedatives to be continued at home.
A 1‐year‐old intact female Bulldog weighing 19.2 kg was presented to the OSU‐VMC by first responders for smoke inhalation and thermal burns from a house fire. Upon presentation, the patient was tachypneic at 60/min with harsh lung sounds diffusely on auscultation. There were multiple partial‐ to full‐thickness burns along the head, neck, and dorsum. After an initial assessment, the patient received analgesia (methadone8, 0.2 mg/kg, IV), sedation (acepromazine4, 0.02 mg/kg, IV), and flow‐by oxygen supplementation.
Upon presentation, arterial CO‐oximetry1 was performed, revealing a moderately increased [14] COHb at 27.2% (RI: 1.3–2.7). HFNOT was initiated within 30 min of presentation using an HFNOT system9 at 1 L/kg/min, an FiO2 of 1.0, and a temperature of 34°C. Thoracic radiographs interpreted by a board‐certified radiologist showed evidence of an unstructured interstitial pattern within the right middle lung lobe, suspected to be NCPE or pneumonitis from smoke inhalation. The patient was bathed to remove soot and ash from the coat, and 1% silver sulfadiazine cream10 was applied topically to burns on the dorsum, lateral abdomen, face, and neck.
Discomfort from facial burns prevented the patient from tolerating nasal cannulas; thus, venous CO‐oximetry1 was rechecked 4 h after the initiation of HFNOT. Improvement was seen in COHb at 3.4% (RI: 1.3–2.7), and the patient was transitioned to an oxygen cage with FiO2 0.45. The FiO2 was weaned overnight, and the patient remained eupneic on room air the next day. Before being discharged on Day 3 of hospitalization, recheck thoracic radiographs showed a new alveolar pattern in the right middle lung lobe with a lobar sign, suspected by the radiologist to represent atelectasis or, less likely, pneumonia or NCPE. The patient was discharged with a nonsteroidal anti‐inflammatory medication, oral sedation, and a topical antimicrobial for outpatient wound care.
The day after discharge, the patient was returned to the hospital for acute dyspnea. At the time of presentation, the patient was cyanotic with an SpO2 value of 79%. Radiographs revealed a new, moderate, diffuse, unstructured interstitial pattern, worse caudally, consistent with NCPE, ARDS, pneumonitis, or thermal injury from the patient's recent smoke inhalation. The patient was readmitted to the hospital, and HFNOT was initiated using a veterinary HFNOT system6 at 1 L/kg/min, an FiO2 of 1.0, and a temperature of 37°C. After an additional 6 days of hospitalization, the patient was discharged, only to return that night for acute respiratory decline after aspiration of respiratory secretions while coughing was witnessed. The patient was hospitalized for COT and supportive care for an additional 2 days and was successfully discharged without occurrence of additional respiratory crises. No delayed neurological signs developed during follow‐up.
During HFNOT, the half‐lives of COHb in each of the three dogs were calculated using the following equation11: t
1/2 = t × ln2 / ln(N
0/N
t), where t denotes the time between the two COHb measurements (N
0, *Nt
*), and N
0 and *Nt
The current series describes the successful use of HFNOT to treat CO poisoning in three dogs. While receiving HFNOT with an FiO2 of 1.0 over 4–8 h, the COHb levels in all three dogs rapidly declined, and no signs of CO poisoning were seen upon discharge. HFNOT is an increasingly common method of treatment in veterinary patients with hypoxemic respiratory failure [8, 15], and the findings from this case series suggest that this modality could be considered as a treatment option for dogs with CO poisoning.
CO poisoning is a potentially life‐threatening condition in people and companion animals [1, 16]. In veterinary medicine, CO exposure commonly results from smoke inhalation during house fires, as seen in the dogs presented in this case series [1, 16]. House fires can also cause direct thermal injury to the upper airways, leading to upper airway obstruction, bronchospasm, and lower airway obstruction from mucosal casts. Combustion of organic material leads to the formation of CO and hydrogen cyanide. Cyanide impairs oxygenation by inhibiting cytochrome oxidase, thus preventing aerobic metabolism [17]. CO competitively binds to Hb with 200–250 times greater affinity than oxygen. Despite tissue hypoxia, however, the respiratory rate may not initially increase until acidosis develops, as the PaO2 remains normal in these patients [1]. CO poisoning may result in acute neurological signs of ataxia, agitation, depressed mentation, loss of consciousness, and seizures due to tissue hypoxia, acidosis, and decreased cerebral oxygen delivery [18]. Delayed neurological signs have also been reported in both human and veterinary medicine [5, 6, 14, 18].
CO‐oximetry provides a means to definitively diagnose CO poisoning, as dissolved oxygen remains unaffected on arterial blood gas analysis, and standard pulse oximetry is falsely increased because of many machines’ inability to differentiate between O2Hb and COHb wavelengths [13, 14, 18]. Mild CO poisoning is associated with COHb levels <20%, and severe poisoning is associated with levels >50% [14], although the veterinary literature is limited [18].
Oxygen therapy with FiO2 of 1.0 is recommended for the treatment of acute CO poisoning [7]. Delivery of oxygen to tissues is improved, and the half‐life of COHb is effectively decreased by promoting the displacement of CO from Hb due to competitive inhibition; thus, the half‐life of COHb decreases as FiO2 increases [2, 7]. On room air (FiO2 of 0.21), the half‐life of COHb is approximately 4–6 h [4]. Supplemental oxygen can be delivered via several methods, including COT, hyperbaric oxygen, HFNOT, and mechanical ventilation [19, 20, 21]. COT comprises flow‐by oxygen, face mask, an oxygen cage, and nasal cannula oxygen [21]. Each method has unique limitations in treating CO poisoning for companion animals. COT in dogs seldomly achieves the desired FiO2 level of 1.0. For instance, flow‐by oxygen, which is generally well tolerated, may only provide an FiO2 of 0.21–0.4 [21]. Face masks and nasal cannulas may provide an FiO2 of up to 0.5–0.6, but the oxygen flow rates required to achieve a higher FiO2 can lead to patient discomfort and are often poorly tolerated in the awake patient. Oxygen cages can provide an FiO2 of up to 0.6, but undesirable fluctuations in FiO2 may occur when the cage is opened to allow direct patient access [20]. By providing an FiO2 of approximately 0.5, COT decreases the half‐life of COHb to 2 h [14]. In people, nonrebreathing masks, noninvasive mechanical ventilation, and continuous positive airway pressure (CPAP) allow for delivery of oxygen with an FiO2 of 1.0, which decreases the half‐life of COHb to 40–80 min [10, 12, 22]. These tightly fitting masks are designed for people and are often not tolerated in veterinary patients, although there are reports of successful use of CPAP helmets in dogs with acute respiratory failure [23]. Hyperbaric oxygen therapy, which provides oxygen with an FiO2 of 1.0 in a pressurized chamber to increase the dissolved oxygen content, has been shown to decrease the half‐life of COHb to 15–30 min in people [7]. Although it has been demonstrated to be more effective than COT and HFNOT in reducing the half‐life of COHb, the availability of hyperbaric oxygen therapy in veterinary hospitals is limited. Thus, finding alternative methods of offering an FiO2 of 1.0 becomes a necessity for treating acute CO poisoning.
Studies in people suggest HFNOT as an alternative to COT for CO poisoning due to its ability to provide an FiO2 up to 1.0 with a higher flow rate [9, 10, 11, 12]. Clinical studies have proven that HFNOT rapidly decreases COHb levels [9, 10, 11, 12]. A retrospective study comparing HFNOT with a conventional face mask in 68 emergency patients with CO poisoning (COHb 20.6%, SD: 8%) showed COHb levels were more rapidly reduced in the first hour with HFNOT (Δ 12.5% ± 4.5% with HFNOT; Δ 6.7% ± 3.7% with conventional face mask) [11]. Additionally, a prospective study of 33 patients with CO poisoning (mean: COHb 22.5%, SD: 8%) found that HFNOT at an FiO2 of 1.0, 60 L/min halved COHb [24] levels in 36.8 min (SD: 9.26) [12]. Subsequent studies reported similar half‐lives: 41.1 min (95% CI: 31–58.4) with HFNOT at an FiO2 1.0, 40 L/min [10] and 48.5 min with HFNOT at an FiO2 of 1.0, 60 L/min [9].
Overall, the half‐lives of COHb reported in human patients treated with HFNOT (36.8–48.5 min) are shorter than those treated with a nonrebreather face mask (74–80 min) and are comparable to those treated with hyperbaric oxygen therapy (24–53 min) [7, 9, 10, 11, 12]. HFNOT also provides enhanced comfort by warming and humidifying inhaled gas [8]. Although there are no specific temperature‐setting guidelines available, a prospective study in people evaluated the comfort of patients at temperatures of 31°C and 37°C, showing improved comfort in hypoxemic patients at the lower temperature [25]. A study in healthy dogs recovering from general anesthesia showed no influence of temperatures between 31°C and 37°C on tolerance of HFNOT [26]; however, the optimal temperature settings in dogs have yet to be investigated. Lower temperatures, ranging from 34°C to 37°C, were chosen for the dogs in this case series in an effort to enhance tolerance and thereby improve the delivered FiO2, effectively reducing COHb.
In addition to the aforementioned benefits, HFNOT offers several physiological advantages over COT that might benefit dogs with smoke inhalation and respiratory diseases. These include reduced dead space, the provision of positive end‐expiratory pressure, and improved humidification and gas exchange [8]. Collectively, these factors demonstrate the potential superiority of HFNOT compared with COT in treating dogs with smoke inhalation and CO poisoning.
Accurate measurement of canine COHb may be limited by the absence of validated blood or pulse CO‐oximeters for canine Hb. This includes the veterinary blood analyzer used in this case series, which, despite its common use in the veterinary literature, may affect the accuracy of COHb half‐life calculations. As such, limited data exist demonstrating the half‐life of COHb in dogs. Wu [21] reported that, compared with a control group of dogs with healthy lungs breathing room air (203 ± 24 min), the half‐life of COHb was prolonged in dogs with induced acute lung injury (275 ± 28 min), which is similar to the 4–6 h reported in people. A half‐life of approximately 125 min was reported in a case series of four dogs and two cats with acute CO poisoning that were treated with an estimated FiO2 between 0.4 and 0.6 using an oxygen cage and nasal cannulas [4]. Recently, a case series described the use of mechanical ventilation and HFNOT in two dogs with CO poisoning [3]. In the dog treated with HFNOT at an FiO2 of 1.0, 1 L/kg/min, the half‐life of COHb was 167 min, while in the dog treated with mechanical ventilation at an FiO2 of 1.0, the half‐life was 150 min. The reported half‐life was derived from arterial blood gas measurements taken during both traditional nasal cannula therapy and HFNOT over the first 7 h. This approach may have resulted in an average half‐life encompassing both methods. The half‐lives of COHb were notably shorter in the dogs presented in this case series, recorded at 79 min for the first case, 86 min for the second case, and 77 min for the third case. Half‐lives in the current case series were based solely on data from the start to the end of HFNOT and likely contributed to the differences observed in the results.
The half‐lives of COHb in the dogs in this series were longer than those included in reports of HFNOT in people. The longer half‐lives reported here may be due to the actual FiO2 being lower than the set FiO2 of 1.0 in the dogs in this case series. Experiments on healthy dogs have shown that HFNOT flow rates of 0.4 and 1 L/kg/min resulted in intratracheal FiO2 of 0.72 and 0.95, respectively [19]. All three dogs in this study started HFNOT at 1 L/kg/min with a set FiO2 of 1.0. The FiO2 delivered should have been close to the set FiO2 of 1.0 based on a previous study [19]; however, other noncontrolled factors, such as tachypnea, open‐mouth breathing, and panting can result in delivery of a system gas–room air admixture, effectively decreasing the delivered FiO2. Studies in healthy dogs and a 3D model have shown that tachypnea can markedly lower the FiO2 during nasal oxygen therapies [27, 28]. A study using HFNOT in healthy dogs demonstrated that with a flow rate of 1 L/kg/min, the delivered FiO2 in non‐panting versus panting dogs was 0.95 and 0.67, respectively [28]. Although the dogs included in the current study were not recorded to be tachypneic, panting is commonly observed and may have contributed to the extended COHb half‐life observed in these dogs. Additionally, two of the three dogs developed pulmonary infiltrates or pulmonary dysfunction. Human and experimental canine studies indicate that individuals with pulmonary dysfunction exhibit a prolonged COHb half‐life after CO poisoning, compared with those with healthy lungs [2, 24]. The pulmonary dysfunction resulting from smoke inhalation may have also affected the observed half‐life of COHb.
In this case series, HFNOT appeared to be safe, well tolerated, and effective in reducing the half‐life of COHb in dogs with CO poisoning caused by smoke inhalation. The half‐life of COHb was shorter than that previously reported, yet it remained longer than the half‐life typically observed in people. Further research with a larger sample of dogs is needed to better understand how HFNOT influences CO poisoning and how it compares to standard or hyperbaric oxygen therapies.
Lauren Robertson: data curation, investigation, methodology, resources, writing – original draft, writing – review and editing. Haley Coughlin: data curation, investigation, resources, writing – original draft. Jiwoong Her: conceptualization, data curation, formal analysis, investigation, methodology, project administration, resources, software, supervision, validation, visualization, writing – original draft, writing – review and editing.
The authors declare no conflicts of interest.