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 Table of Contents  
CASE REPORT
Year : 2020  |  Volume : 7  |  Issue : 1  |  Page : 131-133

A case of near-fatal asthma precipitated by H1N1 pneumonia with critical PCO2 successfully treated by multipharmacological approach


1 King Faisal Hospital, Riyadh, Saudi Arabia
2 Shebin El Kom Teaching Hospital, Shibin El Kom, Egypt

Date of Submission17-Dec-2018
Date of Acceptance20-Aug-2019
Date of Web Publication16-Apr-2020

Correspondence Address:
Talal I Hagag
MD of Critical Care Medicine, Shebin El Kom Teaching Hospital, Md Critical Care, Cairo University, Giza
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/roaic.roaic_109_18

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  Abstract 

We describe a case of prolonged severe hypercapnia with respiratory acidosis occurring during an episode of near-fatal asthma in a 15-year-old boy, followed by complete recovery. After admission to the ICU, despite treatment with maximal conventional bronchodilatation therapy, the clinical picture deteriorated with evident signs of respiratory muscle fatigue. The patient was sedated, intubated, and mechanically ventilated. At 30 min after admission, arterial PCO2 reached 132 mmHg, pH was 6.94, and PO2 was 95 mmHg, and then the measurements repeated after 30 min revealed pH of 6.80, PCO2 of 209 mmHg, and PO2 of 73 mmHg. Oxygenation was initially hypoxic but rapidly maintained, and successful recovery followed without neurological or cardiovascular sequelae. This case shows the cardiovascular and neurological tolerance of a prolonged period of supercarbia in a young patient. The most important lesson to be learned is the extreme importance of maintaining adequate tissue perfusion and oxygenation during an asthma attack. The second lesson is that when conventional bronchodilators fail, the intensivist may resort to the use of drugs such as ketamine, magnesium sulfate, and inhalation anesthesia. In this context, deep sedation and curarization are important, not only to improve oxygenation but also to reduce cerebral metabolic requirements.

Keywords: H1N1, hypercarbia, near-fatal asthma


How to cite this article:
Alzobaidi RA, Hagag TI, Alsharqawy IK, Hasan JH, Rahmatallah MM, Alsamadani SK. A case of near-fatal asthma precipitated by H1N1 pneumonia with critical PCO2 successfully treated by multipharmacological approach. Res Opin Anesth Intensive Care 2020;7:131-3

How to cite this URL:
Alzobaidi RA, Hagag TI, Alsharqawy IK, Hasan JH, Rahmatallah MM, Alsamadani SK. A case of near-fatal asthma precipitated by H1N1 pneumonia with critical PCO2 successfully treated by multipharmacological approach. Res Opin Anesth Intensive Care [serial online] 2020 [cited 2020 May 31];7:131-3. Available from: http://www.roaic.eg.net/text.asp?2020/7/1/131/282585


  Introduction Top


Widespread activity of pandemic A(H1N1) occurred in 2009 and reached its peak a couple of months earlier than the usual seasonal influenza in the northern hemisphere, from April 2009 to January 2010 [1],[2]. The A(H1N1)pdm09 viral infection was considered a mild disease, similar to seasonal influenza. However, many severe and fatal cases were observed not only in the high-risk groups but also among healthy children and young adults during the pandemic waves [3],[4].

Asthma was one of the most common underlying medical conditions among patients hospitalized with A(H1N1)pdm09 viral infection in 2009 worldwide [5]; it is not clear whether A(H1N1)pdm09 viral infection can frequently cause the development of asthma compared with seasonal A(H1N1) or A(H3N3) viral infection. A previous study by Hasegawa et al. [6] showed that seven (31.8%) of 22 asthmatic children with A(H1N1)pdm09 viral infection admitted to a hospital between October and December 2009 were not previously diagnosed with asthma. The sample size of that study is small, and thus, a larger patient population must be studied.

Influenza A viral infection induces the production of interleukin-1β (IL-1β), IL-6, IL-8, tumor necrosis factor-α, histamine, protease, interferon-α, and interferon-γ from airway epithelial cells and other cells including peripheral blood basophils [7]. These proinflammatory cytokines, monokines, and inflammatory substances may contribute to the development of airway inflammation, damaging the barrier function, leading to a subsequent asthma attack.

Camp et al. [8] examined the phenotypic differences in virulence and immune response in A(H1N1)pdm09 virus isolates obtained from hospitalized patients with severe pneumonia. In that study, all viral isolates showed high similarity in nucleic acid sequences in viral gene and replication levels in nasal turbinates and lung, but the isolates’ virulence and host responses in mice varied. Proinflammatory cytokines such as IL-1β and tumor necrosis factor-α and a keratinocyte-derived chemokine were expressed early in mice infected with virulent isolates compared with avirulent isolates, including a vaccine strain of A(H1N1) virus in the 2008–2009 season, A/Brisbane/59/2007. In-vitro experiments demonstrated that a virulent isolate − but not an avirulent isolate − was able to replicate productively in macrophages, suggesting that viral susceptibility to macrophages may be one of the key determinants of their pathogenicity [8].


  Case history Top


We describe a case of prolonged severe hypercapnia with respiratory acidosis occurring during an episode of near-fatal asthma in a 15-year-old boy, followed by complete recovery. After admission to the ICU, despite treatment with maximal conventional bronchodilatative therapy, the clinical picture deteriorated with evident signs of respiratory muscle fatigue. The patient was sedated, intubated, and mechanically ventilated. Magnesium sulfate, ketamine, and midazolam were gradually introduced together with deep sedation, curarization, and continuous bronchodilatative therapy. At 30 min after admission, arterial PCO2 reached 132 mmHg, pH was 6.94, and PO2 was 95 mmHg, and then the measurements repeated after 30 min revealed pH of 6.80, PCO2 of 209 mmHg, and PO2 was 73 mmHg. Thereafter, PCO2 was still elevated (PCO2 184) after 4 h of admission, until it started to decrease to PCO2 of 94 after 5 hours, then gradually increased to PCO2 of 105 after 18 h, then started to reach PCO2 of 60 after 24 h, and after 48 h, the patient’s PCO2 was normal. The patient was extubated, and the results of H1N1 came positive. The patient was started on oseltamivir. Chest radiograph showed severe emphysema. The patient developed hypotension and receive 2 l of normal saline then started levophed infusion 5 mic/minute for 6 hours, then weaned rapidly. Oxygenation was initially hypoxic but rapidly maintained and successful recovery followed without neurological or cardiovascular sequelae. This case shows the cardiovascular and neurological tolerance of a prolonged period of supercarbia in a young patient. The most important lesson to be learned is the extreme importance of maintaining adequate tissue perfusion and oxygenation during an asthma attack. The second lesson is that when conventional bronchodilators fail, the intensivist may resort to the use of drugs such as ketamine, magnesium sulfate and inhalation anesthesia. In this context, deep sedation and curarization are important not only to improve oxygenation but also to reduce cerebral metabolic requirements.


  Discussion Top


Widespread activity of pandemic A(H1N1) 2009 occurred and reached its peak a couple of months earlier than the usual seasonal influenza in the northern hemisphere, from April 2009 to January 2010 [1],[2].

The A(H1N1)pdm09 viral infection was considered a mild disease, similar to seasonal influenza. However, many severe and fatal cases were observed not only in the high-risk groups but also among healthy children and young adults during the pandemic waves [3],[4].

In our study, we observe high PCO2 of 209 mmHg in near-fatal asthma stimulated by H1N1 viral infection. The patient developed severe respiratory acidosis, and with conventional methods, the patient received only intravenous state of sodium bicarbonate 150 ml 8.4% and was on minimal dose of levophed, which was weaned through 6 h. This severe acidosis and hypercarbia did not affect mental status, and the patient was discharged from ICU after 5 days fully conscious oriented without any affection on cognitive state or any residual organ dysfunction. We used protective lung strategy with trial to use low PEEP as possible because patient is asthmatic to avoid as possible auto-PEEP.

In Sunil Kumar Garg, observed a maximum documented PCO2 level of 373 mmHg. While the rise in carbon dioxide tension could be contributed by soda bicarbonate infusion, it appears that a major rise was because of protective lung ventilation and underlying diseased lung as the pCO2 value before starting ventilation and sodium bicarbonate infusion was 100 and 230 mmHg, respectively, and the CO2 value before stopping sodium bicarbonate infusion was 141 mmHg. His recovery was without any obvious adverse consequences.

Several reports emphasize the potential for tolerance to extreme levels of hypercapnia, termed supercarbia.

Mazzeo et al. [9] described complete clinical recovery after an episode of prolonged life-threatening status asthmaticus in an 8-year-old boy. Despite maximal medical therapy involving both conventional and last resort bronchodilator therapies, a progressive respiratory acidosis developed, with a nadir pH of 6.77 and PCO2 of 293 mmHg recorded 10 h after admission. Hemodynamic stability was maintained throughout and no neurologic or other organ dysfunction was detected after eventual complete resolution of status asthmaticus.Urwin et al. [10] reported survival without adverse sequelae after extreme hypercapnia (PCO2 233 mmHg) in an older woman with acute decompensation of chronic obstructive airway disease. To date, however, human trials studying the effect of CO2 per se on outcome in patients with lung injury have not been performed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Amato-Gauci A, Zucs P, Snacken R, Ciancio B, Lopez V, Broberg E et al. Surveillance trends of the 2009 influenza A(H1N1) pandemic in Europe. Euro Surveill 2011; 16:pii:19903.  Back to cited text no. 1
    
2.
Jhung MA, Swerdlow D, Olsen SJ, Jernigan D, Biggerstaff M, Kamimoto L et al. Epidemiology of 2009 pandemic influenza A (H1N1) in the United States. Clin Infect Dis 2011; 52:S13–S26.  Back to cited text no. 2
    
3.
Athanasiou M, Lytras T, Spala G, Triantafyllou E, Gkolfinopoulou K, Theocharopoulos G et al. Fatal cases associated with pandemic influenza A (H1N1) reported in Greece. PLoS Curr 2010; 2:RRN1194.  Back to cited text no. 3
    
4.
Reichert T, Chowell G, Nishiura H, Christensen RA, McCullers JA. Does glycosylation as a modifier of original antigenic sin explain the case age distribution and unusual toxicity in pandemic novel H1N1 influenza? BMC Infect Dis 2010; 10:5.  Back to cited text no. 4
    
5.
Jain S, Kamimoto L, Bramley AM, Schmitz AM, Benoit SR, Louie J et al. Hospitalized patients with 2009 H1N1 influenza in the United States, April-June 2009. N Engl J Med 2009; 361:1935–1944.  Back to cited text no. 5
    
6.
Hasegawa S, Hirano R, Hashimoto K, Haneda Y, Shirabe K, Ichiyama T. Characteristics of atopic children with pandemic H1N1 influenza viral infection: pandemic H1N1 influenza reveals ‘occult’ asthma of childhood. Pediatr Allergy Immunol 2011; 22:e119–e123.  Back to cited text no. 6
    
7.
Yamaya M. Virus infection-induced bronchial asthma exacerbation. Pulm Med 2012; 2012:834826.  Back to cited text no. 7
    
8.
Camp JV, Chu YK, Chung DH, McAllister RC, Adcock RS, Gerlach RL et al. Phenotypic differences in virulence and immune response in closely related clinical isolates of influenza A 2009 H1N1 pandemic viruses in mice. PLoS One 2013; 8:e5660210.  Back to cited text no. 8
    
9.
Mazzeo AT, Spada A, Praticò C, Lucanto T, Santamaria LB. Hypercapnia: what is the limit in paediatric patients. A case of near-fatal asthma successfully treated by multipharmacological approach? Paediatr Anaesth 2004; 14:596–603.  Back to cited text no. 9
    
10.
Urwin L, Murphy R, Robertson C, Pollok A. A case of extreme hypercapnia: implications for the prehospital and accident and emergency department management of acutely dyspnoeic patients. Emerg Med J 2004; 21:119–120.  Back to cited text no. 10
    




 

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