Diphtheritic Polyneuropathy

Piradov, М. А.; Pirogov, V N; Popova, L M; Avdunina, Irina A.

doi:10.1001/archneur.58.9.1438

Cited by 58 publications

(37 citation statements)

References 5 publications

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“…The period between the appearance of first symptom of diphtheria and the development of DP is termed latency, which varies from 10 days to 3 months. [ 3 ] The first indication of neuropathy is paralysis of the soft palate and posterior pharyngeal wall. [ 4 ] Bulbar dysfunction typically develops during the first 2 weeks.…”

Section: Discussionmentioning

confidence: 99%

Diphtheritic polyneuropathy in the wake of resurgence of diphtheria

2015

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Objective:To study the clinical profile and outcome in children with diphtheritic polyneuropathy (DP).Methodology:13 children with polyneuropathy were included in this study. Their demographic profile, age, sex and immunization status were recorded. Detailed clinical and neurological examination was done. Investigations like CSF analysis, NCV studies, MRI brain were done. The results were tabulated and analyzed.Results:All the children presented with bulbar palsy and had h/o membranous tonsillitis. Isolated palatal palsy was seen in 7 children (53%). 6 (46.1%) children developed quadriparesis. 1 child expired and recovery is complete in rest of the 12 children. Children with isolated bulbar palsy recovered within 2 to 4 weeks while children with quadriparesis recovered within 5-6 wks.Conclusions:Any child diagnosed with diphtheria should be followed for 3-6 months in anticipation of neurological complications. DP carries good prognosis hence timely diagnosis and differentiation from other neuropathies is a prerequisite for rational management.

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Section: Discussionmentioning

confidence: 99%

Diphtheritic polyneuropathy in the wake of resurgence of diphtheria

2015

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“…Diphtheria is a contagious disease caused by toxin-producing strains of the bacterium Corynebacterium diphtheriae [ 24 ]. It is a biphasic illness with initial symptoms of fever, throat congestion, neck swelling and ipsilateral palatal weakness followed by diphtheric polyneuropathy.…”

Section: Peripheral Neuropathy and Polyradiculoneuropathymentioning

confidence: 99%

“…The latency in development of diphtheritic polyneuropathy varies from 18 to 46 d after the initial infection. It is an acute demyelinating polyneuropathy, occurs in about 20% of patients with diphtheria[ 24 ]. The classic features of include accommodation disturbances, convergence or pupillary light reflex disturbance, anisocoria, ptosis, mydriasis, malfunction of extraocular muscles and dysfunction of the other cranial nerves followed by quadriparesis[ 24 ].…”

Section: Peripheral Neuropathy and Polyradiculoneuropathymentioning

confidence: 99%

“…Improvement in cranial nerves occurs with evolving motor disturbance in the trunk and extremities. Autonomic dysfunction is common in diphtheritic polyneuropathy, with the incidence ranging from 36% to 100% in severe diphtheritic polyneuropathy[ 24 ]. Diphtheria antitoxin is ineffective if administered after one or two days of diphtheritic symptoms.…”

Section: Peripheral Neuropathy and Polyradiculoneuropathymentioning

confidence: 99%

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Practical approach to the patient with acute neuromuscular weakness

Nayak¹

2017

WJCC

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Acute neuromuscular paralysis (ANMP) is a clinical syndrome characterized by rapid onset muscle weakness progressing to maximum severity within several days to weeks (less than 4 wk). Bulbar and respiratory muscle weakness may or may not be present. It is a common neurological emergency which requires immediate and careful investigations to determine the etiology because accurate diagnosis has significant impact on therapy and prognosis. Respiratory failure caused by neuromuscular weakness is considered as more critical than lung disease because its development may be insidious or subtle until sudden decompensation leads to life threatening hypoxia. Also, the arterial blood gas finding of severe hypoxemia, hypercapnia, and acidosis may not be apparent until respiratory failure is profound. Hence, the requirement for respiratory assistance should also be intensively and promptly investigated in all patients with neuromuscular disease. The disorder is classified based on the site of defect in motor unit pathway, i.e., anterior horn cells, nerve root, peripheral nerve, neuromuscular junction or muscle. Identification of the cause is primarily based on a good medical history and detailed clinical examination supplemented with neurophysiologic investigations and sometimes few specific laboratory tests. Medical history and neurological examination should be focused on the onset, progression, pattern and severity of muscle weakness as well as cranial nerves testing and tests for autonomic dysfunction. Associated non neurological features like fever, rash or other skin lesions etc. should also be noted. Globally, Guillain-Barré syndrome is the most frequent cause of ANMP and accounts for the majority of cases of respiratory muscles weakness associated with neuromuscular disorders. Newly acquired neuromuscular weakness in intensive care unit patients consist of critical illness polyneuropathy, critical illness myopathy and drug induced neuromuscular weakness which may arise as a consequence of sepsis, multi-organ failure, and exposure to certain medications like intravenous corticosteroids and neuromuscular blocking agents.

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“…Although rapid administration of diphtheria antitoxin reduces the case-fatality rate for respiratory diphtheria, antitoxin administration after day 1 of diphtheritic polyneuropathy shows no benefit ( 22 ). Many countries no longer store diphtheria antitoxin for therapeutic use.…”

Section: Clinical Aspects Of Diphtheritic Polyneuropathymentioning

confidence: 99%

Detection of Diphtheritic Polyneuropathy by Acute Flaccid Paralysis Surveillance, India

Mateen¹,

Bahl²,

Khera³

et al. 2013

Emerg. Infect. Dis.

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Diphtheritic polyneuropathy is a vaccine-preventable illness caused by exotoxin-producing strains of Corynebacterium diphtheriae. We present a retrospective convenience case series of 15 children (6 girls) <15 years of age (mean age 5.2 years, case-fatality rate 53%, and 1 additional case-patient who was ventilator dependent at the time of last follow-up; median follow-up period 60 days) with signs and symptoms suggestive of diphtheritic polyneuropathy. All cases were identified through national acute flaccid paralysis surveillance, which was designed to detect poliomyelitis in India during 2002–2008. We also report data on detection of diphtheritic polyneuropathy compared with other causes of acute flaccid paralysis identified by this surveillance system.

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Diphtheritic Polyneuropathy

Cited by 58 publications

References 5 publications

Diphtheritic polyneuropathy in the wake of resurgence of diphtheria

Diphtheritic polyneuropathy in the wake of resurgence of diphtheria

Practical approach to the patient with acute neuromuscular weakness

Detection of Diphtheritic Polyneuropathy by Acute Flaccid Paralysis Surveillance, India

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