Hypercapnia: what is the limit in paediatric patients? A case of near‐fatal asthma successfully treated by multipharmacological approach

Mazzeo, Anna Teresa; Spada, A.; Praticò, C; Lucanto, T; Santamaria, L. B.

doi:10.1111/j.1460-9592.2004.01260.x

Cited by 40 publications

(20 citation statements)

References 31 publications

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“…Our calculated target Pa CO 2 was greater than that accepted in normal clinical practice within neonatal intensive care units. Although adult humans may tolerate extreme levels of hypercapnia without adverse effects (37,49), the population of human infants most prone to develop BPD are at particular risk of developing intracranial hemorrhage, retinopathy of prematurity and neurodevelopmental impairment. Their risk of developing the latter morbidities may be increased by hypercapnia (12,17,48), and any future studies designed to test the potential benefits of a less conservative Pa CO 2 than previously used (9) would need to be undertaken with an appropriate degree of caution.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic effects of hypercapnia on chronic lung injury and vascular remodeling in neonatal rats

Masood

Man

Lau

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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Permissive hypercapnia, achieved using low tidal volume ventilation, has been an effective protective strategy in patients with acute respiratory distress syndrome. To date, no such protective effect has been demonstrated for the chronic neonatal lung injury, bronchopulmonary dysplasia. The objective of our study was to determine whether evolving chronic neonatal lung injury, using a rat model, is resistant to the beneficial effects of hypercapnia or simply requires a less conservative approach to hypercapnia than that applied clinically to date. Neonatal rats inhaled air or 60% O2 for 14 days with or without 5.5% CO2. Lung parenchymal neutrophil and macrophage numbers were significantly increased by hyperoxia alone, which was associated with interstitial thickening and reduced secondary crest formation. The phagocyte influx, interstitial thickening, and impaired alveolar formation were significantly attenuated by concurrent hypercapnia. Hyperoxic pups that received 5.5% CO2 had a significant increase in alveolar number relative to air-exposed pups. Increased tyrosine nitration, a footprint for peroxynitrite-mediated reactions, arteriolar medial wall thickening, and both reduced small peripheral pulmonary vessel number and VEGF and angiopoietin-1 (Ang-1) expression, which were observed with hyperoxia, was attenuated by concurrent hypercapnia. We conclude that evolving chronic neonatal lung injury in a rat model is responsive to the beneficial effects of hypercapnia. Inhaled 5.5% CO2 provided a significant degree of protection against parenchymal and vascular injury in an animal model of chronic neonatal lung injury likely due, at least in part, to its inhibition of a phagocyte influx.

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Section: Discussionmentioning

confidence: 99%

Therapeutic effects of hypercapnia on chronic lung injury and vascular remodeling in neonatal rats

Masood

Man

Lau

et al. 2009

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…Ketamine infusions have been used in patients with near-fatal asthma, in combination with other bronchodilator therapies. 161 …”

Section: Ketaminementioning

confidence: 99%

Severe Acute Asthma Exacerbation in Children: A Stepwise Approach for Escalating Therapy in a Pediatric Intensive Care Unit

Nievas

Anand

2013

The Journal of Pediatric Pharmacology and Therapeutics

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OBJECTIVES An increasing prevalence of pediatric asthma has led to increasing burdens of critical illness in children with severe acute asthma exacerbations, often leading to respiratory distress, progressive hypoxia, and respiratory failure. We review the definitions, epidemiology, pathophysiology, and clinical manifestations of severe acute asthma, with a view to developing an evidence-based, stepwise approach for escalating therapy in these patients. METHODS Subject headings related to asthma, status asthmaticus, critical asthma, and drug therapy were used in a MEDLINE search , supplemented by a manual search of personal files, references cited in the reviewed articles, and treatment algorithms developed within Le Bonheur Children's Hospital. RESULTS Patients with asthma require continuous monitoring of their cardiorespiratory status via noninvasive or invasive devices, with serial clinical examinations, objective scoring of asthma severity (using an objective pediatric asthma score), and appropriate diagnostic tests. All patients are treated with β-agonists, ipratropium, and steroids (intravenous preferable over oral preparations). Patients with worsening clinical status should be progressively treated with continuous β-agonists, intravenous magnesium, helium-oxygen mixtures, intravenous terbutaline and/or aminophylline, coupled with high-flow oxygen and non-invasive ventilation to limit the work of breathing, hypoxemia, and possibly hypercarbia. Sedation with low-dose ketamine (with or without benzodiazepines) infusions may allow better toleration of non-invasive ventilation and may also prepare the patient for tracheal intubation and mechanical ventilation, if indicated by a worsening clinical status. CONCLUSIONS Severe asthma can be a devastating illness in children, but most patients can be managed by using serial objective assessments and the stepwise clinical approach outlined herein. Following multidisciplinary education and training, this approach was successfully implemented in a tertiary-care, metropolitan children's hospital. INDEX TERMS asthma, child, critical care, infant, respiratory failure, status asthmaticus J Pediatr Pharmacol Ther 2013;18(2):88-104

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“…The rate of alveolar ventilation has a major impact on systemic CO 2 and oxygen levels. 2,3 Most commonly, P aCO 2 levels are altered in response to changes in alveolar ventilation, where respiratory depression (ie, due to sedatives or narcotics), 4 airway obstruction, 5 and increased V D can drive P aCO 2 higher. 6 Although the rate of carbon dioxide production generally remains constant, hypermetabolic states such as sepsis, malignant hyperthermia, thyroid crisis, and overfeeding can lead to elevations in CO 2 levels ( Table 1).…”

Section: Introductionmentioning

confidence: 99%

Carbon Dioxide in the Critically Ill: Too Much or Too Little of a Good Thing?

Marhong

Fan

2014

Respir Care

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Hypercapnia and hypocapnia commonly complicate conditions that are present in critically ill patients. Both conditions have important physiologic effects that may impact the clinical management of these patients. For instance, hypercapnia results in bronchodilation and enhanced hypoxic vasoconstriction, leading to improved ventilation/perfusion matching. Hypocapnia reduces cerebral blood volume through arterial vasoconstriction. These effects have also been exploited for therapeutic aims. In patients with traumatic brain injury (TBI), hypocapnia is often utilized to control intracranial pressure. However, this effect is not sustained, and prolonged hypocapnia increases the risk of mortality and severe disability in patients with TBI. Hypercapnia and hypercapnic acidosis are common consequences of lung-protective ventilation in ARDS. Hypercapnic acidosis reduces ischemic lung injury and preserves lung compliance, but concern has arisen over hypercapniainduced immunosuppression and the potential for bacterial proliferation in sepsis. Experimental studies suggest that buffering hypercapnic acidosis attenuates these effects, whereas hypocapnia appears to potentiate lung injury through increased capillary permeability and decreased lung compliance. Several areas of uncertainty surround the role of hypercapnia/hypocapnia in treating TBI and ARDS. Current data support recommendations to avoid hypocapnia in treating TBI, with the exception of emergent treatment of elevated intracranial pressure, while awaiting definitive management. Permissive hypercapnia is commonly accepted as a consequence of lung-protective ventilation in ARDS, but there is insufficient evidence to support the induction of hypercapnic acidosis in clinical practice. Buffering hypercapnic acidosis should be considered only for a specific clinical indication (eg, hemodynamic instability). For clinicians choosing to buffer hypercapnic acidosis, tris-hydroxymethyl aminomethane is recommended over sodium bicarbonate, as it is more effective in correcting pH and is not associated with increased carbon dioxide production. Future studies should aim to address these areas of uncertainty to help guide clinicians in the therapeutic use and management of hypercapnia/hypocapnia in critically ill patients.

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Hypercapnia: what is the limit in paediatric patients? A case of near‐fatal asthma successfully treated by multipharmacological approach

Cited by 40 publications

References 31 publications

Therapeutic effects of hypercapnia on chronic lung injury and vascular remodeling in neonatal rats

Therapeutic effects of hypercapnia on chronic lung injury and vascular remodeling in neonatal rats

Severe Acute Asthma Exacerbation in Children: A Stepwise Approach for Escalating Therapy in a Pediatric Intensive Care Unit

Carbon Dioxide in the Critically Ill: Too Much or Too Little of a Good Thing?

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