Pakistan J. Med. Res.

Vol. 41 No.2, 2002

 

Clinical evaluation of patients with acute flaccid motor weakness

Farid Ullah Shah, Mohammad Salih, Iftikhar Ahmed Malik

Department of Medicine, Federal Government Service Hospital, Islamabad

 

SUMMARY

 

Objectives: To differentiate Guillain Barre’ syndrome from hypokalemicperiodic paralysis on basis of clinical features and simple laboratory investigations like serum potassium level, E.C.G, blood gases analysis.

Patients and methods: Patients presented between January 1999 to June 2000 to the department of Neurology of Pakistan Institute of Medical Sciences Islamabad were included in this study.

Patients more than 13 years of age and of both sexes, who were conscious, with lower motor neuron type of weakness, which developed within a period of four weeks with no sensory level, were included in this study. All patients who were unconscious, who were having sensory level, in whom weakness developed in a period of more than four weeks, patients with diabetic neuropathy, acute renal failure, porphypria and lead poisoning were excluded.

Results: Out of 33 patients, 22 (66.7%) were suffering from Guillain Barre’ syndrome ( G B S) , 5(15.1%) from hypokalemic periodic paralysis (HPP), 4(12.1%) from hypokalemic paralysis ( HP) with hypokalemia secondary to renal tubular acidosis type-1 and 2(6.1%) from critical illness neuropathy(CIN).

All 22 patients with GBS developed distal weakness except one patient.  Serum potassium level was 3.9 to 4.6 mmol/l (mean level 4.72 mmol/l). Respiratory failure was present in 9(40.9%) patients; bulbar palsy in 13 (59.1%) patients and 2(9.1%) patients expired.

All patients with HPP developed proximal as well as distal weakness.  Serum potassium level was 1.5-mmol/l to2.5mmol/l  (mean 2.06 mmol/l). Two (40%) patients developed respiratory failure and 2(40%) bulbar palsy. One (20%) patient expired.  Family history and history of repeated episodes of weakness was positive in 3(60%) patients. While in 2(40%) patients, there   was no family history and no past history of weakness. 

Cause of hypokalemia was renal tubular acidosis type -1, in all HP patients. All developed both proximal as well as distal weakness.  Serum potassium level was 1.9 to 2.9 mmol/l  (mean 2.22 mmol/l).   Respiratory failure was present in 2(50%) patients and 2(50%) patients developed bulbar palsy.  Two (50%) patients expired.

Critical illness neuropathies were present in two patients. Both patients were on mechanical ventilator. One patient (50%) expired.

Conclusion: Certain clinical and laboratory criteria differentiate HPP from GBS, which includes Positive family history and similar episodes of weakness in the past, rapid onset of weakness in hours, quick recovery in 24 to 72 hours, and low serum potassium during the episodes of weakness.

Key words: Guillain Barre’ syndrome- G B S. hypokalemic periodic paralysis –HPP.  hypokalemic paralysis – HP.  Critical illness neuropathy-CIN

 

INTRODUCTION

 

C

ommon causes of acute peripheral nervous system diseases leading to acute symmetrical motor paralysis are Guillain Barre’ syndrome, hypokalemic periodic paralysis and hypokalemic paralysis.The leading cause of acute flaccid paralysis is the acute paralytic neuropathy which is clinically diagnosed as GBS1. In two third of cases, an infection, either clinically overt, or evident by serum titer rise, precedes the neuropathy by 1 to 4 weeks. Herpes virus infections (Cytomegalo virus, Epstein Barr virus, and Mumps virus) account for a large proportion of virus trigged cases. Other cases appear to be triggered by Campylobacter jejuni gastroenteritis and Mycoplasma pneumoniae2-4. A small proportion, less than 5%, occurs within 1 to 4 weeks of a surgical procedure. GBS also occurs on the background of lymphoma, including Hodgkin’s disease, and lupus erthematosus. The clinical features of GBS include areflexic motor paralysis with or without sensory disturbance, the weakness rapidly and symmetrically progresses to affect the legs predominantly, and arms. The maximum weakness occurs in 4 to 8 days after the onset of weakness. The cerebrospinal fluid protein is raised by the end of first week of symptoms5-7. Eighty percent of the cases are demyelinating and inflammatory. An unusual variant, the Miller Fisher syndrome, present with ataxia, areflexia, and external ophthalmoplegia, but the weakness appears later in its course8. Other variants are notable for an axonal pattern of electro diagnostic findings and axonal pathology with little inflammation1

 

The aim of this study was to differentiate GBS from HPP on the bases of clinical features and simple laboratory investigations, because the treatment and the outcome of both the diseases is quite different

 

Hypokalemic periodic paralysis is autosomal dominant trait in two third and sporadic in one third of the cases7. So, there may be a family history and past history of episodic weakness.  Onset is before 25 years of age, usually in the first or second decade. Weakness affects the proximal limb muscles more than the distal ones. Involvement of ocular, bulbar, or respiratory muscles is rare, but fatal. Meals high in carbohydrates or sodium can provoke attacks. Reflexes are hypoactive, but intact. Low serum potassium during the episode of weakness is diagnostic for hypokalemic paralysis7, but one should also consider the possibilities of HP with hypokalemia of Secondary causes, like vomiting, diarrhea, diuretic abuses, renal tubular acidosis type 1 and type 2,Bartter’s syndrome and Liddle’s syndrome. 

 

PATIENTS AND METHODS

 

Patients more than 13 years of age and both sexes, who were conscious, with lower motor neuron type of weakness, which developed within a period of four weeks with no sensory level, were included in this study.                                                                                                    

 

All patients who were unconscious, were having sensory level, in whom weakness developed over a period of more than four weeks, patients with diabetic neuropathy and acute renal failure were excluded from the study. Patients with Porphypria were excluded  on the basis of history, clinical findings and urinary porphobilinogen level. Lead poisoning was also excluded on the basis history of exposure and clinical finding.

 

Patients with acute flaccid motor weakness were assessed clinically from the history of weakness, extent of weakness, with or without tingling sensation or numbness in limbs, with or without the preceding history of upper respiratory tract infection or diarrhea. 

 

Extent of weakness was assessed according to the Functional Disability Scale score. Respiratory stability was assessed from single breath count, rate and depth of respiration, cyanosis and blood gases analysis. Cardiac stability was assessed from rate and rhythm of pulse, blood pressure and electrocardiogram9 (Table-1).

 

Table 1:  Functional disability score (15) 

 

Scale score

Functional disability

    0

    1

    2

    3

    4

    5

 

    6

Healthy.

Having minor symptoms and signs.

Able to walk > 10m without assistance.

Able to walk > 10m with a walker or support.

Bed ridden.

Requiring assisted ventilation for at least part of the day.

Dead

 

Investigations included complete blood count, peripheral blood picture, urea, creatinine, serum sodium and potassium level, ECG, blood gasses analysis, nerve conduction studies, and urinary porphobilinogen level (in suspected cases only).The data was analysed on Epi-info statistical software and probability was calculated through Chi square testing

 

Diagnostic criteria for Guillain Barre’ Syndrome:

 

Except the CSF finding we used Asbury diagnostic criteria for the diagnosis of GBS, which are: (I)–Features required for the diagnosis. (A)-Progressive motor weakness of more than one limb. (B)-Areflexia. (II)-Features strongly supportive of the diagnosis. (A) –(1)-Progression within 4 weeks. (2)-Relative symmetry. (3)-Mild sensory symptoms or signs. (4)-Cranial nerves involvement. (5)-Recovery within four weeks of progression stopping. (6)-Autonomic dysfunction. (7)-Absence of fever at onset. (B)-(1)-Raised CSF protein. (2)-CSF mononuclear leucocytes less than 10 per micrometer. (C)-Electro diagnostic study strongly supportive of the diagnosis (nerve conduction slowing or block). (III)-Features causing doubt on the diagnosis. (1)- Pronounced asymmetry of weakness. (2) –Persistent bowel or bladder dysfunction. (3) –Bladder or bowel dysfunction at onset. (4)- More than 50 mononuclear leucocytes in CSF. (5)- Presence of polymorph nuclear leucocytes in CSF. (6)- Sharp sensory level. Features that rule out the diagnosis. (1)-Current history of hexacarbon misuse. (2)-Abnormal porphyrin metabolism. (3)-Recent diphtheria infection.(4)-Features clinically consistent with lead neuropathy.(5)-Purely sensory syndrome.(6)-Definitive diagnosis of poliomyelitis, botulism, hysterical paralysis, or toxic neuropathy. Nerve conduction study suggestive of demyelinating or axonal neuropathy type of pattern was used as a strong supportive investigation for GBS. Demyelination is associated with marked slowing of conduction velocity and marked prolongation of distal latency. Reduced amplitude with preserved latency and conduction velocity is the feature of axonal neuropathy 9.

 

Diagnostic criteria for Hypokalemic periodic/ Hypokalemic paralysis:

 

Predominantly proximal weakness, weakness developed within a period of minutes to hours, with diminished or intact reflexes, rare involvement of bulbar and respiratory muscles, low serum potassium during episode of weakness, response to treatment within 24-72 hours. 

All patients with GBS were treated with supportive treatment which included, mechanical ventilator for respiratory failure, nasogastric feeding for bulbar palsy, antibiotics according to the culture sensitivity for chest infection, cardiac monitoring and treatment for cardiac arrythmias, low molecular heparin or subcutaneous unfractional heparin for prevention of pulmonary embolism and postural changes and physiotherapy for prevention of pressure sores. Potassium was replaced immediately in patients with hypokalemic paralysis.Acute treatment is replacement of potassium at rate not exceeding more than 40-mmol/ hour or 200-mmol/ day in normal saline or manitol {never in 5%dextrose}, while monitoring the ECG, serum potassium and muscle strength of patients.  

 

RESULTS

 

Out of 33 patients, 22 (66.7%) were suffering from GBS,  (one with miller Fisher syndrome), 5(15.1%) from HPP, 4(12.1%) from HP of secondary hypokalemia and 2(6.1%) from CIN. Out of 22 patients with GBS, 13 were male, between the age group of 13 to 56 years (mean age 30 years), 9 were female, between the age group of 26 to 70 years (mean age 30 years). Duration of illness before admission was 1 to 15 days (mean duration 5.5 days). Disability scale at the time of admission was 5/6 in 9 patients, 3/6 in 3 patients and 2/6 in 10 patients. All patients had distal weakness except one. Serum potassium level was 3.9 to 4. 6 mmol/l (mean level 4.72 mmol/l). Eight patients (36.4%) had preceding respiratory tract infection and o5 (22.7%) had diarrheal illness. Duration of onset of weakness was from 08 hours to 07 days (mean 2.67 days) (Table 2).

 

Table 2:  Demographic data and acute complications of GBS.

 

Variables

No. (%)

P values

Total no. Of patients

22  (66.7)

-

Age range (Yr.)

13-70

-

Mean age (Yr)

30

-

Sex M/F (no.)

13/9

-

DOIBP (days)

1-15

-

Mean duration (days)

5.5

-

Acute complications:

 

-

Respiratory failure

9   (40.9)

.85

Bulbar palsy

1  (59.1)

.45

Facial palsy

10  (45.5)

.013

Assisted ventilation

9  (40.9)

.85

Chest infection

9  (40.9)

.85

 Mortality

2  (9.1)

.023

DOIBP: Duration of illness before presentation.

 

Nine patients (40.9%) developed respiratory failure (P=.85) and 13 (59.1%) bulbar palsy (P=.45) (Fig 1, 2).

  

Figure: 1:  Frequency of respiratory failure in patients with acute flaccid motor weakness

GBS = Guillain Barre’ syndrome

HPP = Hypokalemic periodic paralysis

HP   = Hypokalemic  paralysis

       

 

 

 

 

 

 

 

 

 

 

Figure 2: Incidence of bulbar palsy in patients with acute flaccid motor weakness

GBS = Guillain Bare’ syndrome

HPP = Hypokalemic periodic paralysis

HP   = Hypokalemic  paralysis

 

Two patients (9.1%) expired (P=.023) (Fig 3),

Figure: 3  Mortality in patients with acute flaccid motor  weakness

GBS = Guillain Bare’ syndrome

HPP = Hypokalemic periodic paralysis

HP   = Hypokalemic  paralys

 

01 (4.5%) from cardiac arrhythmia and 01 (4.5%) from hypovolemic shock secondary to upper gastro intestinal bleeding with septicemia and disseminated intravascular coagulation. Nerve conduction study showed acute demyelinating type of neuropathy in 19 patients (86.3%) and axonal type of neuropathy in 3 patients (13.7%). Bilateral facial palsy with lower motor neuron type of weakness was present in 10 patients (45.4%) (P=.013). Disability scale at discharge was 4/6 in 7 patients, 2/6 in 2 patients and 1/6 in 10 patients. Total hospital stay was 7 to 56 days (mean stay 32 days)

 

Five patients (15.1%) with flaccid motor weakness had HPP. Three were males and 2 females between the age group of 13 to 24 years (mean age 19.6years). Duration of illness before admission was 6 to 24 hours (mean 24 hours). Disability scale at the time of admission was 4/6 in 3 patients and 5/6 in 2 patients. Serum potassium level was 1.5 2.5 mmol/l (2.06 mmol/l) (Table 3).

 

Table 3: Demographic data and acute complications of hypokalemic periodic paralysis.

 

Variables

No. (%)

P values

Total no. of patients

5(15.1%)

-

Age range (Yr.)

13-24

-

Mean age

19.6

-

Sex M/F (no.)

3/2

-

DOIBP (hours)

6-24

-

Mean duration (hrs)

24

-

Acute complications:

 

-

Respiratory failure

2 (40%)

.92

Bulbar palsy

2 (40%)

.46

Facial palsy

0

.09

Assisted ventilation

2 (40%)

.92

Chest infection

2 (40%)

.92

Mortality

1 (20%)

.201

DOIBP: Duration of illness before presentation

 

Two (40%) patients developed respiratory failure (P=.92) and bulbar palsy (P=.46) (Fig 1, 2). Both the patients were put on ventilator; one patient expired (P=.201) (Fig 3) due to progressive heart block and cardiac arrhythmias. All the patients presented with proximal as well as distal weakness, with diminished reflexes in 2 and absent reflexes in 3 patients. Weakness developed in 8 to 48 hours (mean 23.25 hours). Duration of recovery was 24 hours in 3 patients and 72 hours in one patient. There was positive family history and past history of weakness in 03 patients  (60%) and no such history in 2 patients (40%). Total hospital stay was 4 to 7 days (mean 4.8 days). Disability scale at discharge was 0/6 in all 03 patients.

 

Four patients  (12.1%)were suffering from HP with hypokalemia due to renal tubular acidosis type -1.All patients were between the age group of 20 to 24 years (mean age 20.5). Two patients were males and 2 females. Duration of illness before admission was 8 to 72 hours (mean 46.6 hours) (Table 4).

 

Table 4:  Demographic data and acute complications of hypokalemic paralysis.

 

Variables

No. (%)

P values

Total no. of patients

4(12.1%)

-

Age range(Yr.)

20-24

-

Mean age

20.5

-

Sex M/F(no.)

2/2

-

DOIBP (hrs)

8-72

-

Mean duration(hrs)

46.6

-

Acute complications:

 

-

Respiratory failure

2 (50%)

.72

Bulbar palsy

2 (50%)

.83

Facial palsy

0

.139

Assisted ventilation

2 (50%)

.72

Chest infection

2 (50%)

.72

Mortality

2 (50%)

.09

DOIBP: Duration of illness before presentation

 

Disability scale at the time of admission was 3/6 in 2  and 5/6 in 2 patients. Serum potassium was 1.9 to 2.9 mmol/l (mean 2.22mmol/l). One patient was presented with the second episode of paralysis. Two patients (50%) developed  respiratory failure (P=.72) and bulbar palsy (P=.83) (Fig1,2).  Two patients (50%) expired (P=.09) (Fig 3). Causes of death were cardiac arrhythmias in one patient and severe metabolic acidosis due to gradual deteriorating renal function in one patient. Total hospital stay was 7 days in both patients. Disability scale at the time of discharge was 0/6 in both patients.

 

Two (6.1%) patients with flaccid weakness were suffering from CIN, one male aged 40 years with multiple organs failure syndrome as a complication of surgery and second a female 26 years of age with meningococcal meningitis and septicemia. Both patients were on mechanical ventilator. Female patient with meningococcal meningitis and septicemia recovered with left foot drop, while the male patient with laprotomy expired from cause other than the neuropathy.

 

Discussion

 

G B S is the common cause of acute flaccid motor paralysis1. G B S is a heterogeneous disorder, which encompasses clinical subtypes. Miller Fisher syndrome, which was present in one patient with ataxia, external ophthalmoplegia, areflexia and marked proximal weakness, is the common variant of GBS8.  Weakness develops within a period 04 of weeks, usually within 4 to 8 days1,5. While in our study the mean duration of onset of weakness from the onset of symptoms was 2.76 days. Weakness is usually symmetrical, but some time one group of muscles may be involved first. Weakness progressively ascends to evolve the proximal muscles as well as the respiratory and bulbar muscles, leading to respiratory and bulbar weakness. In our study 40.9% patients developed respiratory failure and 59.1% developed bulbar palsy. Cranial nerve palsy is the differentiating feature of GBS. In our study bilateral lower motor neuron type of facial palsy was present in 45.4% of the cases.  The common complications of GBS are, respiratory failure, bulbar palsy, and autonomic failure leading to tachycardia, arrhythmias and labile hypertension, pulmonary embolism due to deep venous thrombosis, decubetus ulcer and permanent disability. Main causes of mortality are respiratory failure, chest infection, cardiac arrhythmias and pulmonary embolism1,5,10.  In our study 9.1% patients expired, 4.5% from cardiac arrhythmia and 4.5% from hypovalemic shock secondary to upper gastrointestinal bleeding with septicemia and disseminated intravascular coagulation. Polio virus, coxsackie   virus, echo virus and other entero virus are the causes of motor neuron disease of anterior horn cells leading to flaccid motor weakness. Motor weakness due to polio and other entero virus infection can be differentiated from GBS on the basis of epidemic occurrence, fever, meningeal symptoms, purely motor and asymmetrical flaccid motor weakness. But, rarely can cause symmetrical flaccid motor weakness simulating GBS. The nerve conduction study is decisive with normal conduction velocity and denervative EMG in motor neuron disease. CSF protein is raised in both in GBS as well as in polio; with lymphocytes range 100-200 cells per micrometer in polio and less than 10 cells per micrometer in GBS11. More than 50 mononuclear cells in the CSF will cause doubt in the diagnosis of GBS.

 

The main aim of this study was to differentiate GBS from HPP and HP, because the treatment and the out come of two diseases are different.

 

Hypokalemic periodic paralysis is autosomal trait in two third of the cases and is due to a defect in the calcium channel of skeletal muscle, while in one third of the cases it is sporadic. So, we can differentiate Hypokalemic periodic paralysis from GBS on the basis of family history of periodic weakness, history of episodic weakness, but the episodes of weakness may be daily to yearly, Proximal as well as distal muscles weakness, with predominant proximal muscles weakness and hypoactive but intact reflexes, rare involvement of respiratory and bulbar muscles, short duration of onset of weakness in hours and rapid recovery usually complete within 24 hours and rarely 72 hours and Low serum potassium below 3.5 mmol/l during the episode of weakness and no cranial nerve palsies, although on occasion serum potassium may be normal7,9. In our study all patients developed proximal as well as distal weakness. Mean duration of onset of weakness from the onset of symptoms was 23.25 hours.  Past history of weakness and positive family history was present in 60% of cases. While in 40% of cases there was no past history of weakness and positive familyhistory, probably these were sporadic cases.  Respiratory failure and bulbar palsy was present in 40% (2/5) of our cases with a mortality of 20% due to cardiac arrhythmias. Major complications of periodic paralysis are cardiac arrythmias, respiratory failure, bulbar palsy and disability due repeated episodes of weakness7,9. Hpokalemia of secondary causes can also cause weakness,with low serum potassium. So, one should rule out the possibilities of secondary causes of hypokalemia like diarrhea, vomiting, diuretic abuses, Cushing syndrome, Conn’s syndrome, ACTH producing tumor, steroids therapy, renal tubular acidosis, Barrter’s syndrome and Liddle’s syndrome.

 

Critical illness Polyneuropathy is differentiated from GBS on the bases of its association with persistent sepsis and multiple organs dysfunction syndrome (MODS). Like GBS, limbs are weak, flaccid with reduced or absent reflexes and predominantly motorneuropathy and nerve conduction studies will confirm axonal damage. Critical illness neuropathies can be differentiated fromaxonal type of GBS on these criteria *GBS is the primary neurological reason for admission on the intensive care unit, critical illness neuropathies on the other hand developed during a patient’s stay on the intensive care unit for another reason. *Infectious symptoms such as fever and diarrhea have usually subsided before the clinical features of GBS appear.  *Unlike GBS,CSF protein is normal or minimally raised. *IgG ganglioside antibodies GM1, GM1b,GD1a are absent in critical illness neuropathies12. Recovery is expected in 1 to 6 months with supportive treatment13. Critical illness neuropathies in Critical ill patients must be differentiated from pressure palsies.  In pressure palsies the peripheral nerves like axillary, median, radial, ulnar, peronial nerves are evolved at the entrapment site leading to asymmetrical paralysis with pressure sores, involvement of both sensory and motor components and the nerve conduction study is showing slowing of conduction velocity or conduction block between proximal and distal stimulation sites across the damage site.  Conduction block is severe attenuation of amplitude and sensory nerve action potentials evoked or recorded above the site of injury compared to those evoked or recorded below and slowing of motor and sensory conduction across the damage area 14

 

CONCLSSION

 

Though the clinical presentation of patients with hypokalemic periodic paralysis were similar to GBS, that is, they presented with flaccid motor weakness, reduced or absent reflexes, involving respiratory failure [40%] and bulbar palsy (40%), was also equally high. However, certain clinical and laboratory criterias can differentiate hypokalemic periodic paralysis from GBS, which includes: family history was present in 60% of cases; history of episodic weakness was present in 60% of cases, maximumweakness developed in hours and all patients recovered in 24 to 72 hours and the recovery was complete in all patients, serum potassium level was low (3.5 mmol/l) in all patients during the episodes of weakness.  Partial recovery and bilateral low motor neuron type of facial palsy was very helpful in the diagnosis of GBS.     

 

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