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Diphtheritic Polyneuropathy
Clinical Analysis of Severe Forms
Michael A. Piradov, MD, PhD, DMSc;
Victor N. Pirogov, MD;
Lubov M. Popova, MD;
Irina A. Avdunina, MD
Arch Neurol. 2001;58:1438-1442.
ABSTRACT
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Background Diphtheritic polyneuropathy (DP) is a dangerous complication of diphtheria,
especially its severe forms with bulbar, respiratory tract, and circulatory
disturbances. However, the clinical picture of severe forms of DP is practically
unknown.
Objective To investigate the clinical features and peculiarities of the course
of severe forms of DP.
Patients Thirty-two patients with severe forms of DP.
Results The first symptoms of DP developed in most patients 3 to 5 weeks after
the onset of diphtheria. The cranial nerves were involved in all patients,
most frequently nerves IX and X (32 patients); VII (28 patients); III, IV,
and VI (27 patients); and XI (27 patients). One third of the patients had
quadriplegia. The remaining patients had quadripareses. Of the 32 patients,
24 underwent artificial ventilation. All patients had sensory signs, proprioceptive
more often than superficial. Autonomic disturbances were observed also in
all patients. Only 2 of the 32 patients died.
Conclusions A direct indication for tracheotomy and artificial ventilation in patients
with DP is a decrease of the vital capacity of the lungs below the traditional
16 mL/kg body weight or the development of the paralytic closure of the larynx
against the background of the increasing weakness of the respiratory muscles.
Characteristic of severe forms of DP is the phenomenon of the oppositely directed
change in the neurological symptoms in the second month of the disease: the
restoration of the function of the cranial nerves against the background of
the further increase of the motor disturbances in the extremities and trunk.
Special attention and care should be taken of patients during the period of
the appearance of the episodes of vascular collapses—between the fourth
and seventh weeks of DP.
INTRODUCTION
FROM 1990 to 1995, the epidemic of diphtheria broke out in the former
Soviet Union. The number of patients reached 90% of all cases documented in
the world during this period. More than 125 000 humans were infected
with diphtheria, and 4000 of them died. More than 97 000 cases with 2500
fatal outcomes took place in Russia,1 where
the epidemic was accompanied by a pronounced increase in the number of patients
with one of its most dangerous complications, diphtheritic polyneuropathy
(DP).2, 3 The incidence of DP is
directly proportional to the severity of diphtheritic intoxication, and it
may occur in 68% of the total number of diphtheritic patients.4, 5, 6
The most dangerous are the severe forms of DP, with bulbar, respiratory tract,
and circulatory disturbances. Mortality due to these forms of DP surpassed
50%, even in the specialized hospitals.3, 7
Although paralysis of the diaphragm was known earlier as a sign leading to
100% lethality of patients with DP (without artificial ventilation [AV]),
the data on clinical manifestations of severe forms of DP and the life-threatening
role of respiratory insufficiency in this disease are scarce. The high diphtheritic
lethality resulted from the inefficiency of respiratory therapy during previous
epidemics, most of which broke out before the 1950s, when the modern devices
of AV became widespread. This article describes the clinical presentation
and the course of the disease in the patients with severe forms of DP, most
of whom had the respiratory tract disturbances and needed AV.
SUBJECTS AND METHODS
The subjects were 32 patients with severe forms of DP (18 men and 14
women; mean ± SD age, 44 ± 4 years; age range, 21-54 years)
admitted to our hospital from January 1, 1990, to December 31, 1997. All patients
had toxic diphtheria with cervical subcutaneous fat edema spread down to the
clavicles and below them (28 and 4 patients, respectively). Laboratory diagnostic
testing was performed, with microbiological isolation of the causative pure
culture of diphtheria and identification of its basic morphological, biochemical,
and toxic features in infectious disease hospitals. Bacteriologic tests revealed Corynebacterium diphtheriae gravis in 24 patients and Corynebacterium diphtheriae mitis in 6. In 2 patients,
diphtheria was diagnosed in the infectious inpatient departments based on
clinical and epidemiological data. Only 1 of 32 patients was vaccinated with
a single dose of antidiphtheritic serum 1 year before infection.
Diphtheria was located in the stomatopharynx (23 patients), the stomatopharynx
and the larynx (3 patients), the stomatopharynx and the nose (4 patients),
the nose and the larynx (1 patient), and the stomatopharynx and hand skin
(1 patient). Treatment with diphtheritic antitoxin was delayed because of
the untimely admission of the patients into the infectious disease clinics
(Figure 1). Three patients received
no specific treatment. In addition to antidiphtheritic serum, the patients
in the infectious disease clinics received antibiotics, cardiovascular drugs,
and corticosteroid hormones. The early phase of diphtheria was accompanied
by soft palate (15 patients) and accommodation (8 patients) pareses, which
lasted for no more than 2 weeks. The somatic complications (myocarditis and
nephrosis) were observed in 30 and 27 of the patients, respectively. On average,
the symptoms of DP were manifest 30 days after the onset of diphtheria. At
the time of hospital admission, 15 patients needed AV, while other patients
either were bedridden or could walk no more than 5 m. Nine more patients needed
AV during the first 2 weeks after admission. In total, AV was performed in
24 of the patients.
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Figure 1. Time of instituting treatment
with diphtheritic antitoxin.
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Neurological status and vital capacity (VC) were determined daily in
all patients. A radiological examination of diaphragm motility was performed
2 to 3 times during inpatient treatment. Data are given as mean ± SD
unless otherwise indicated.
RESULTS
LATENCY AND THE FIRST SYMPTOMS OF DP
The period between the appearance of the first symptoms of diphtheria
and the development of DP was termed latency. It
varied from 18 to 46 (mean, 30 ± 8) days. The first symptoms of DP
were numbness in the gingivae, tongue, and face (24 patients); paresthesia
in the fingers and toes (32 patients); and dysphonia with dysphagia (32 patients).
In 23 patients, the first symptoms of DP appeared 3 to 5 weeks after the onset
of diphtheria, while in other patients they were manifest 6 to 7 weeks after
the onset. The latency was shorter in the patients with the most severe neurological
disturbances, which dictated AV (Figure 2).
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Figure 2. Duration of latency in patients
with diphtheritic polyneuropathy. The mean ± SD latency in those who
underwent artificial ventilation (AV) was 28.0 ± 6.1 days; in those
who did not undergo AV, 35.0 ± 8.8 days.
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THE BASIC SYMPTOMS OF DP
All patients had pareses of motor cranial nerves, weakness of respiratory
and abdominal muscles, quadriparesis and quadriplegia with areflexia and muscular
hypotonia, peripheral sensory disturbances, pain syndrome in the arms and
legs (mostly pronounced to the end of DP month 2), and autonomic disturbances.
Half of the patients had sensory ataxia.
CRANIAL NERVE DISTURBANCES
The bilateral disturbances of cranial nerves III, IV, VI, VII, IX, and
XII were most frequently observed (Table
1). The clinical signs of lesions in cranial nerves I, II, and VIII
were absent. The oculomotor disturbances were manifested as ptosis, anisocoria,
and diplopia (Table 2). These
abnormalities were observed in all patients undergoing AV and in half of the
other patients. The oculomotor disturbances during DP were short compared
with those of other cranial nerves. The sensory and motor functions of cranial
nerve V were disturbed in 17 and in 11 of the patients, respectively. Palpation
of the trigger zones of cranial nerve V was painful in 13 of the patients
undergoing AV during the development of DP symptoms. A lesion of the facial
nerves was observed in 28 of the patients, including all patients undergoing
AV and 4 not undergoing AV. A lesion of cranial nerves IX and X was manifested
during weeks 3 to 5 of diphtheria by dysphonia, dysphagia, respiratory insufficiency,
and asphyxia. Dysphagia was combined with excessive salivation and regurgitation
of fluid food via the nose, its aspiration into the trachea leading to a cough
attack and asphyxia. These disturbances dictated nasal feeding in the patients
who were and were not undergoing AV for 56 ± 3 and 37 ± 4 days,
respectively. Aphagia and aphonia occurred in 24 of the patients. In these
patients, laryngoscopy revealed the development of 2 variants of laryngeal
paralysis: (1) paralytic laryngospasm (n = 14) and (2) paralytic laryngostenosis
with 50% narrowing of the laryngeal lumen (n = 10). In 5 of the 14 patients,
the paralytic laryngospasm developed on day 22 of DP (on the average), and
was the main reason to perform AV. These patients had no signs of paralysis
of the diaphragm, and their VC was 38.2 ± 5.3 mL/kg. In the other 9
patients, the paralytic laryngospasm was observed from day 23 of DP (on the
average) during AV necessitated by paralysis of the diaphragm and a diminished
VC (10.1 ± 1.6 mL/kg).
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Table 1. Cranial Nerve Disturbances in 32 Patients With Diphtheritic
Polyneuropathy
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Table 2. Oculomotor Disturbances in 32 Patients With Diphtheritic Polyneuropathy
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The paralytic laryngospasm was observed in the patients with the most
severe symptoms of DP. The durations of nasal feeding of the 14 and 10 patients
with and without paralytic laryngospasm were 62 ± 4 and 50 ±
3 days, respectively, while the durations of AV were 50 ± 3 and 33
± 4 days, respectively. Only 2 patients with paralytic laryngospasm
died, although it was not the cause of their death. Paralysis of cranial nerve
XI was observed in all patients undergoing AV and in only 3 not undergoing
AV. Paresis of cranial nerve XII was observed in all patients undergoing AV,
while paralysis of this nerve occurred in 2 patients. Of 8 patients not undergoing
AV, 3 had pareses of cranial nerve XII.
RESPIRATORY TRACT DISTURBANCES
Respiratory tract disturbances of mixed genesis were observed in all
patients. We observed the disturbances of cough reflex; obstruction in the
conducting airways; aspiration of nose-pharyngeal and stomatopharyngeal content
due to pareses and paralyses of the pharynx, larynx, and tongue combined with
pareses and paralyses of the respiratory muscles; and bronchopulmonary pathological
features. The respiratory tract disturbances appeared during weeks 1 to 3
of DP, and they were most pronounced during week 4. Artificial ventilation
was performed in 24 of the patients. Paralysis of the diaphragm was observed
in all patients who needed AV and in 2 who did not need AV. The total paralysis
of respiratory muscles was observed only in 1 patient. The duration of AV
ranged from 17 to 62 days (mean, 43 days).
MOTOR DISTURBANCES
The motor disturbances in the extremities were observed during weeks
2 to 3 of DP, and they slowly developed during weeks 6 to 9, reaching the
maximum on day 51 ± 10 of DP. Proximal quadriparesis was revealed in
most patients (n = 26). In 11 of the patients, quadriplegia was observed,
while other patients had pronounced quadripareses. All patients had muscular
hypotonia and tendinous areflexia. The patients could walk only 4 months after
the onset of DP. There was an inverse relationship between DP latency and
the period needed to restore motor function: a longer latency corresponded
to earlier regression of motor disturbances (Figure 3).
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Figure 3. Duration of latency and time of
quadriparesis regression. In 29 patients, we attempted to predict the day
of onset of quadriparesis regress (Y) from the day diphtheritic polyneuropathy
started (X) using simple regression analysis. X (mean ± SD, 30.3 ±
6.9 days) and Y (mean ± SD, 61.9 ± 9.4 days) are normally distributed
(according to the Shapiro-Wilks W test) continuous variables. The assumptions
of simple linear regression were verified. The slope (-0.86) of the
regression line significantly differs from 0, indicating that Y tends to decrease
as X increases (95% confidence interval, -1.25 to -0.47; t27 = -4.19; P<.001; Y = 87.87 -
0.86X; r= -0.63; r2 = 0.39). We
used statistical software (STATISTICA ‘99; StatSoft Inc, Tulsa, Okla)
for the calculations.
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SENSORY DISTURBANCES
All patients demonstrated hypoesthesia and hyperesthesia, disturbances
in joint position sense, tactile discrimination, and vibration. Hypoesthesia
and hyperesthesia accompanied by the elements of hyperpathia of the distal
parts of the extremities (usually to the level of the upper thirds of the
forearms and legs) were maximal on day 47 ± 13 of DP. The joint position
sense, tactile discrimination, and vibration were most frequently disturbed
in the distal regions to the level of the elbow and knee joints. They were
most pronounced on days 52 ± 11 and 42 ± 12 of DP, respectively.
Sensory ataxia was observed in half the patients.
AUTONOMIC DISTURBANCES
The autonomic disturbances were observed in all patients. They included
sinus tachycardia (32 patients); arterial hypotension (32 patients) leading
to collapses (11 patients); retention of urine (11 patients); pronounced xeroderma
and hyperkeratosis (24 patients); and hyperemia and hyperhidrosis in the face,
neck, and chest, at the background of the general paleness of the skin (20
patients). A sudden decrease of arterial pressure occurred during weeks 4
to 7 of DP, and it continued for 3 to 10 days (Figure 4). During this period, all patients needed continuous injections
of dopamine hydrochloride. In 2 patients, cardiac intensive care was needed,
although an electrocardiogram revealed neither short-term damage to the myocardium
nor arrhythmia. Retention of urine developed on day 37 ± 4 of DP, and
it was observed in 10 patients undergoing AV and in 1 not undergoing AV. In
all these patients, persistent catheterization of the urinary bladder was
needed for 5 to 14 days.
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Figure 4. Time of development of blood pressure
decreases in patients with diphtheritic polyneuropathy (DP).
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CEREBROSPINAL FLUID
Cerebrospinal fluid (CSF) was examined in 27 patients, and CSF pressure
was measured with open-tube manometry in 24 patients at different periods
of the disease (days 17-68 of DP). In 9 of the patients, the CSF pressure
was enhanced from 200 to 440 mm H2O. The CSF protein level was
0.103 ± 0.073 g/dL (range, 0.015-0.283 g/dL), and it did not depend
on the duration and severity of the disease. Albumin-cytologic dissociation
was observed in 21 of the patients. The CSF cell count did not surpass 12
cells per cubic millimeter (lymphocytes and neutrophils).
COURSE OF THE DISEASE
Disturbance and recovery of neurological functions during DP were characterized
with certain regularities. The cranial nerves were affected first, cranial
nerves IX and X being disturbed most severely. Nasal feeding was needed as
early as day 11 of DP (on average). The duration of nasal feeding varied from
26 to 87 days. As a whole, functional recovery of the cranial nerves was accomplished
during weeks 5 to 10 of DP. The motor disturbances appeared during weeks 2
to 3 of DP, and they slowly aggravated to day 51 ± 10 of DP. Quadriplegia
was observed in 11 patients, while other patients had severe quadripareses.
Regression of motor disturbances began on day 61 ± 12 of DP. Thus,
the phenomenon of counterchanges of the neurological symptoms was observed
during the second month of the disease: the functional recovery of cranial
nerves developed simultaneously with aggravation of motor disturbances in
the trunk and extremities. The regress of sensory disturbances started during
weeks 12 to 14 of DP.
OUTCOME OF THE DISEASE
Despite severity and a long-term character of the neurological disorders,
a virtually complete regression of neurological symptoms was observed in 30
patients. Two patients died of the development of pneumonia complicated by
pyopneumothorax and acute cardiovascular insufficiency combined with hemorrhagic
syndrome.
COMMENT
Analysis of the development and the course of severe forms of DP showed
that neurological symptoms resulted from the toxic forms of diphtheria. None
of our patients was treated with antidiphtheritic serum on day 1 of the occurrence
of diphtheria. It is known that diphtheria toxin penetrates into Schwann cells
and binds to them as early as 1 hour postinjection, inducing the latent development
of polyneuropathy.8 A severe lesion of the
peripheral nervous system caused by the diphtheria toxin led to the development
of DP accompanied with disturbances of the vital functions. Our data corroborate
the existence of a direct relationship between the intensity of diphtheritic
intoxication and the probability of the development of severe neurological
disorders, thereby stressing the importance of immediate administration of
the antidiphtheritic serum.
It was believed that manifestation of neurological disorders in the
most immediate period of diphtheria foreshadowed the development of DP.4, 5 However, less than half of our patients
had the neurological disturbances (such as paresis of the soft palate and
accommodation disorder) in the immediate phase of diphtheria, although all
patients had somatic complications (myocarditis and/or nephrosis). It seems
that cardiac and renal disturbances, not the early neurological symptoms,
are most indicative of the possibility of DP development.
In all patients, DP was clinically manifested after some latency, which
varied from 18 to 46 days. Other data5, 7, 9, 10
attest to a pronouncedly greater period of 5 to 16 weeks between the onset
of diphtheria and the manifestation of the first DP symptoms.
This longer latency probably resulted from a mild course of the disease
in the described patients, in whom the most vital functions were not disturbed.
We saw, for the first time to our knowledge, the existence of the reverse
relationship between DP latency and the onset of the regression of neurological
symptoms: the longer the latency, the earlier the regression of motor disturbances.
Correspondingly, the most severe clinical forms of DP were observed in the
patients with a short latency.
Many studies showed that the first symptoms of DP are paresis of the
soft palate and paresthesia in the distal parts of the extremities. Patients
with paresthesia on the face, gingivae, and tongue are rarely described.6 By contrast, we observed these symptoms accompanied
with paresis of the soft palate and paresthesia in the distal parts of the
extremities in 24 of our patients. Previously, the sensory disturbances were
reported only for the innervation area of cranial nerve V.6
By contrast, we revealed not only the sensory abnormalities of cranial nerve
V but also the corresponding motor disturbances of cranial nerve V, which
can be explained by the severity of the disease.
It is generally considered that accommodation disturbances are characteristic
of DP, while malfunction of extraocular muscles is a rare symptom lasting
for no more than 2 weeks.4, 9, 10
In our study, these abnormalities were observed in 27 of the patients for
5 to 8 weeks, and half of these patients had accommodation paresis and a lesion
of the extraocular muscles. A lesion of the facial nerve was revealed in 28
of the patients during weeks 7 to 8 of DP, while other researchers4, 10, 11 observed similar lesions
in 8% to 35% of patients; these lesions lasted for no longer than 3 weeks.
We showed, for the first time to our knowledge, the development of 2
variants of laryngeal paralysis during weeks 3 to 5 of DP; these were manifest
as laryngospasm and 50% laryngostenosis. Laryngoscopy revealed the role of
laryngeal paralysis in the development of respiratory tract disturbances during
DP. In 5 of the patients, laryngospasm was the major reason to start AV, although
the mean VC of these patients was 38 mL/kg, and paresis of respiratory muscles
did not reach the critical level. Therefore, extrathoracic obstruction of
the airways resulting from laryngeal paralysis can be fatal even before the
development of pronounced paresis of the respiratory muscles. Laryngeal paralysis
during DP is the reason to start AV, even in patients with a sufficient VC.
Laryngospasm is an unfavorable factor in the course of DP.
Respiratory muscle pareses are the life-threatening neurological problem
during DP. In one patient, we observed the total respiratory paresis unknown,
to our knowledge, in the medical literature. Malfunction of the respiratory
muscles was manifest during weeks 1 to 3 of DP, and it attained its maximum
only during weeks 3 to 4, which dictated the use of long-term AV (43 days
on average). Therefore, AV of patients with DP who have a combination of bronchopulmonary
pathological features and pronounced long-term malfunction of respiratory
muscles must be performed via tracheotomy without the intubation stage.
Dysfunction of the cranial nerves appeared earlier and developed more
rapidly than quadriparesis, which is a typical feature of DP. This period
of DP is sometimes referred to as the "cranial stage."12
Quadriplegia in patients with DP is reported extremely rarely.10, 13
In our study, it was observed in 11 of the patients. In most of these patients
(n = 26), the proximal type of quadriparesis developed. In contrast, the distal
type of quadriparesis is characteristic of less severe forms of DP.10, 13 In our patients, the maximum of motor
disturbances was observed at the end of month 2 of DP, after which regression
of motor disturbances started, so the patients could walk without assistance
2 months later. Satisfactory reversibility of neurological disorders during
diphtheria is well-known, although such long-term disturbances were observed
rarely.4, 10, 13 The
self-restricting course of DP indicates that the immune cells do not actively
participate in the development of the pathological process, as evidenced by
the absence of inflammatory changes in the nerves.14, 15
The prolonged course of neurological disorders reflects the peculiarities
of remyelinization, which does not restore the myelin even 2 months after
the onset of DP.14 Analysis of severe forms
of DP revealed the phenomenon of the opposite changes of neurological symptoms
during the second month of the disease: functional recovery of cranial nerves
proceeded simultaneously with the development of motor disturbances in the
extremities. This phenomenon is probably explained by peculiarities of damage
and remyelinization in different nerves,14, 15
and further study should elucidate its nature. The proprioceptive disturbances
were also observed in the patients without vital functional disorders.1, 4, 7, 9, 10, 11
However, these disturbances were much more prolonged and pronounced in patients
with severe DP.
The monitoring of basic variables of systemic hemodynamics showed that
weeks 4 to 7 of DP is the period when the circulatory collapses are most probable.
The absence of immediate myocardial damage and arrhythmic episodes during
this period indicates that a lesion of the autonomic nerve fibers is the main
cause of the sudden decreases in arterial pressure.
The modern methods of intensive care made it possible to prevent death
in our patients and to study the course of severe forms of DP aggravated by
respiratory insufficiency. The unfavorable economic conditions in many countries
combined with high migration and communication without intensity increase
the probability of new diphtheria outbreaks. Neurologists should always keep
in mind the possibility of a diphtheritic cause of polyneuropathy. The timely
diagnosis of DP is a prerequisite for the rational treatment and beneficial
outcome of this disease, even in the most severe cases.
AUTHOR INFORMATION
Accepted for publication June 12, 2001.
From the Neurointensive Care Department, Institute of Neurology, Russian
Academy of Medical Sciences, Moscow.
Corresponding author and reprints: Michael A. Piradov, MD, PhD, DMSc,
Institute of Neurology, Russian Academy of Medical Sciences, Volokolamskoye
Shosse 80, 123367 Moscow, Russia (e-mail: mpiradov{at}neurology.med.ru).
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