Medical Emergiencies aboard an Airplane, what to do differen

[Doczilla]

Ok now this is an interesting thread, could it be possible that this individual could be suffering from Central Neuological HyperVentilation it is not as uncommon as one would think, what exactly was the disability, the cramping you describe would it be possible that this was "Midwives sign" perhaps a calcium related problem ?

Someone hear hoofbeats? Must be zebras.

Central neurogenic hyperventilation in a conscious patient without a brainstem infarct, invasive tumor, monster brain injury, or serious CNS infection is rarely, if ever, reported. In head traumas, this signals impending herniation, in which case your patient would not be conscious.

Holy crap. Hypocalcemia?!

NO. Look, you've got to look at common things being common, and neither of the above is common. A person on a plane who is hyperventilating with carpopedal spasm after getting a bonk on the head by a falling cane is not herniating, particularly if she's alert enough to complain of a headache.

Less time Googling, more time at the bedside, Grasshopper.

'zilla

[tniuqs]

[quote="Doczilla

Someone hear hoofbeats? Must be zebras.

'zilla

[tniuqs]

Just for interest sake:

Introduction

Central neurogenic hyperventilation (CNH) is usually seen in deeply comatose patients following severe brain damage from head injury, intracranial infection or stroke. Its characteristic features are severe respiratory alkalosis, significantly reduced arterial carbon dioxide tension, and increased arterial oxygen tension. The diagnosis requires exclusion of pulmonary, cardiac, and metabolic disorders that can result in hyperventilation (1). CNH is very rarely encountered in an awake patient. We describe a fully awake woman with a pontine lesion who presented with CNH.

Case report

A 46-year old woman presented with occipital headache of 2 weeks' duration. There was no fever, loss of consciousness or fits. She was fully alert, with normal higher functions. There was no meningism. She had bilateral facial nerve palsy, right-sided trigeminal sensory impairment and quadri-hyperreflexia, compatible with a pontine lesion. Routine hematological and biochemical tests were normal. Chest radiograph, electroencephalogram (EEG), and CT scan of the brain were normal. Cerebrospinal fluid (CSF) analysis revealed protein 32 mg/dI, lymphocytes 85/ml, and a normal glucose level. CSF was negative for acid-fast bacilli, fungi, malignant cells, and polymerase chain reaction for Mycobacterium tuberculosis. She was commenced on anti-tuberculous therapy, along with systemic steroids.

The headache initially settled with treatment, but recurred three weeks later. She was quite conscious and alert. She had developed a right-sided motor fifth cranial nerve palsy, bilateral cerebellar signs and ataxia of gait. She was noticed to be hyperventilating, and this persisted unaltered even during sleep. The respiratory rate varied from 36 to 44/minute. Rebreathing through a paper bag, and intravenous diazepam had no effect on the over breathing. Cardiovascular and respiratory systems were normal. Basic blood tests, chest radiograph, electrocardiogram and echocardiogram remained normal. Lung function tests could not be performed reliably because of marked hyperventilation. Arterial blood gases done while breathing room air, showed marked respiratory alkalosis with partial compensation: pH 7.64, pO2 131 mmHg, pCO2 13 mmHg, O2 saturation 99.6%, and HCO3 24 mmol/l.

Further investigations were performed to determine the aetiology of the pontine lesion. Ultrasound scan of the abdomen and bone marrow trephine biopsy were normal. Antinuclear antibody, dsDNA, lupus anticoagulant, anticardiolipin antibody, C-ANCA and P-ANCA were negative, Mycoplasma and viral antibodies were negative. A repeat CT scan of the brain revealed a small enhancing lesion in the left parieto-occipital region. MRI of the head showed multiple T2-weighted lesions scattered throughout the cerebral cortex and brainstem, including the pons. A CT-guided steriotactic biopsy of the parieto-occipital lesion revealed non-specific infiltration of cerebral tissue with chronic inflammatory cells. Eleven days after admission, she became fatigued and confused, and required mechanical ventilation. She lapsed into a coma and succumbed. Consent for a pathological postmortem was denied by the family.

Discussion

A review of the literature showed that here were 19 published cases of CNH in awake patients. They included primary cerebral lymphoma (7 cases), astrocytoma (6 cases), medulloblastoma (1 case), invasive laryngeal carcinoma (I case), systemic histiocytosis (1 case), and unknown pathology, 3 cases (2,3,4,5). Primary cerebral lymphoma is an uncommon variety of extra-nodal nonHodgkin's lymphoma (2), but its high incidence in CNH is an interesting finding.

The mechanism of causation of CNH is controversial. It is believed to arise from lesions of the pontine reticular formation resulting in interruption of the inhibitory pathways to the medullary respiratory centre (6). This view is supported by the demonstration of a pontine lesion in most cases. However, this has been questioned following the report of a case with a lesion in the midbrain (7), and another in the medulla (4). Two other cases without any demonstrable brainstem lesions have also been reported (1). Another hypothesis is that abnormal amounts of lactic acid produced by the brainstem neoplasm stimulate the chemoreceptors in the medulla resulting in hyperventilation. However, positron emission tomography (PET) studies have ruled out this theory (7).

In patients with primary cerebral lymphoma, regression of tumour and remission of hyperventilation has been achieved by brain irradiation, steroids and chemotherapy (2). The prognosis was poor in patients with astrocytoma and where the pathology was unknown (1,2). CNH eventually results in fatigue and death. Hyperventilation has been shown to respond to intravenous infusion of sodium bicarbonate, and to morphine and methadone (8).

EDIT as per request;

References

Pauzner R, Mouallem M, Sadeh M, Tadmo R, Farfel Z. High incidence of primary cerebral lymphoma in tumour induced central neurogenic hyperventilation. Archives of Neurology 1989; 46: 510-3.

Shibata Y, Meguro K, Narushima K, Shibuya F, Doi M, Kikuchi Y. Malignant lymphoma of the central nervous system presenting with central neurogenic hyperventilation. Journal of Neurosurgery 1992; 76: 696-700.

Gottlieb D, Michowitz SD, Steiner 1, Wald U. Central neurogenic hyperventilation in a patient with medulloblastoma. European Neurology 1987; 27: 51-4.

Dubaybo BA, Afridi 1, Hussain M. Central neurogenic hyperventilation in invasive laryngeal carcinoma. Chest 1991; 99: 767-9.

Hool GJ, Marsh HM, Groover RV, Burgert EO, Simmons PS, Reese DF. Episodic central neurogenic hyperventilation in an awake child with systemic hystiocytosis. Journal of Paediatrics and Child Health 1993; 29: 154-5.

Plum F, Swanson AG. Central neurogenic hyperventilation in man. Archives of Neurology and Psychiatry 1959; 81: 535-49.

Bateman DE, Gibson GJ, Hudgson P, Tomlinson BE. Central neurogenic hyperventilation in a conscious patient with a primary cerebral lymphoma. Annals of Neurology 1985; 17: 402-5.

Salvesan R. Pontine tumour with central neurogenic hyperventilation: pharmacologic intervention with morphine sulfate and correlative analysis of respiratory, sleep, and ocular motor dysfunction. Neurology 1990; 40: 1715-20.

[ERDoc]

My guess is that since this is a disabled Marine there is probably a degree of PTSD. The hit to the head triggered something that caused her to hyperventilate. Hyperventilation caused the carpopedal spasms by a transient hypocalcemia (specifically ionized calcium) due to hypocarbia. You can also see Trousseau's and Chevosteks (sp?) Signs with hyperventilation.

[NREMT-Basic]

Doc-

I didnt see the notation in the case history that this woman was a disabled marine, but perhaps I lost it in the shuffle. The case reports note quite clearly it seems that she tested negative for tuberculosis. If this was in fact the case, why was the patient started on an anti-tubercular therapy?

[AnthonyM83]

I also do not identify myself to get in the mile high club as I don't have any aspirations of becoming a member without my wife gaining membership with me.

Well, some say three's a crowd...not me...it's company.

BTW, never implied you ask for drinks. Just thinking that it'd be easier for a lawyer to prove employment if you (editorial you) fly frequently, because after you help someone and get a drink, it's possibly understood you might get something the next time you help someone on a flight. Versus someone who helps out for the first time and later gets a drink for the first time, because he has no knowledge of this supposed "employment" at the time he rendered aid. There was no empoyment relationship at that time.

Edit: And this is only because the topic about the lawyer's advice was brought up.

[ERDoc]

Doc-

I didnt see the notation in the case history that this woman was a disabled marine, but perhaps I lost it in the shuffle. The case reports note quite clearly it seems that she tested negative for tuberculosis. If this was in fact the case, why was the patient started on an anti-tubercular therapy?

My comments were in reference to the post by mediccjh about his experience, not about the case report. As far as the case report, I'd like to see the reference. You should never post something that someone else has written without a reference. I can't explain why she was started on anti-TB meds. It definitely would not be high on my differential. The CSF results do concern me, but it's hard to know what to make of them given an almost entirely nonspecific workup. As you can see case reports are not very useful in practice. They are published because they are so rare and interesting. If they weren't so rare and interesting no one would care and they would not be published. They are a way for someone to say, "Hey, check this out. You will never believe what I had the other day." But that's just my opinion. They never alter anyone's practice and you will likely never see what they are talking about in your practice.