Acute neuromuscular paralysis is one of the common neurological emergencies, of which Guillain Barre Syndrome GBS remains the most common cause. This syndrome presents with acute ascending muscle weakness and loss of deep tendon reflexes DTR , often preceded by distal paresthesia and back pain. However, a severe hypokalemia may have a similar presentation and put the treating physician in dilemma. We report a year-old previously healthy man, who presented with acute areflexic ascending quadriparesis associated with impending respiratory failure.
This followed a one day history of frequent diarrhea, vomiting and low grade fever. A provisional diagnosis of GBS was given by the treating physician and the patient was intubated for ventilatory support. A few hours later the serum potassium and magnesium were reported to be very low, so the patient was given parenteral potassium chloride KCl , later supplemented with magnesium.
Even though severe hypokalemia related muscle weakness reported rarely, it is a potentially treatable and correctable cause of neuromuscular weakness. Guillain-Barre syndrome includes a spectrum of autoimmune polyradiculoneuropathy in which peripheral nerve myelin is the major target. The prototype variant is acute inflammatory demylinating polyneuropathy AIDP.
Guillain-Barre syndrome commonly follows minor infectious illness like acute gastroenteritis, upper respiratory infection, some vaccinations. Although GBS is the most common cause of acute flaccid quadriparesis in the United States, a retrospective study done by Zenebe et al highlights the importance of GBS as a cause of peripheral nerve disease in Ethiopia as well 4.
The typical presentation of GBS is acute progression of ascending limb weakness and areflexia with minimal sensory deficit and intact bladder function, unless there is associated severe autonomic dysfunction at presentation 2,7. However, patients presenting to emergency department with acute flaccid weakness may have a wide differential diagnosis including neurological disorders such as GBS and myasthenia gravis, metabolic diatheses including hypokalemia, and infectious causes.
Since any of the above may have symptoms similar to those found in GBS, a rapid certain diagnosis may be difficult. Even though acute hypokalemia induced areflexic weakness is a rare disorder, it is a potentially treatable and reversible cause of acute ascending areflexic muscle weakness 9.
A 42 year-old healthy male was brought to emergency room of Tikur Anbessa Specialized Tertiary Hospital TASH by his family with rapidly progressing, ascending weakness of all four extremities of 10 hours duration. During that time he was also having increasing difficulty breathing. He gave a history of frequent watery diarrhea, vomiting, and low grade fever a day prior to onset of the weakness. This followed attendance at a wedding ceremony in Addis Ababa, and at the onset of diarrhea with subsequent weakness he visited a local health center that referred him to TASH after they gave him unspecified oral medications for diarrhea.
The patient denies any history of recent vaccination, flu symptoms or exposure to barium or any other drugs. He denied history of similar weakness in the past and had no history of chronic illness. His social history is pertinent for occasional khat chewing but he denies drinking any alcohol.
There was no history of loss of consciousness, abnormal body movement, urinary retention or incontinence. On physical examination the patient was fully conscious, but in acute respiratory distress wearing a face mask with high oxygen flow supplementation. On respiratory system examination there was visible use of use of accessory muscles and single breath count of 8. Examination of sensory and cranial nerves as well as spinal vertebrae revealed no abnormality.
No evidence of Tick bites on body examination. After considering this examination with his history of ascending weakness and preceding acute gastroenteritis, a provisional diagnosis of ascending GBS with impending type 2 respiratory failures was made, and the patient was intubated for ventilatory support.
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He was kept in the emergency department since there was no bed available in the intensive care unit ICU. His complete blood count was normal. Arterial blood gas testing was not available. Following this patient was given parenteral potassium chloride 40milliequivalents in milliliters normal saline over 4 hours supplemented with magnesium sulfate. After 4 hours potassium was infused at typical maintenance levels. He was then able to support himself and chat with his family.
Plans for further testing including nerve conduction studies, spinal MRI, and CSF analysis were deferred, and he was kept in the emergency department overnight, with complete metabolic evaluation planned for the next morning. However, the patient suddenly sustained cardiac arrest and passed away, due to cardiac arrest secondary to fatal cardiac arrhythmia, despite minute Cardio respiratory resuscitation CPR , as patient was given standard replacement dose of KCL the risk of hyperkalemia induced cardiac arrhythmia is low.
Acute neuromuscular weakness with associated respiratory failure is not an uncommon problem to emergency departments all over the world, including Ethiopia. The pain group consisted of GBS patients with medical records indicating pain symptoms. Of the GBS patients, 6 were excluded due to coma and communication difficulty, and 1 patient was excluded due to the presence of chronic pain 3 months prior to the onset of GBS.
Of the patients enrolled, 87 patients had the complain of pain Fig. The basic demographic and clinical characteristics of the GBS patients are summarized in Table 1. The pain characteristics of the 87 GBS patients who reported pain are summarized in Table 2.enter
Guillain-Barré syndrome: Symptoms, causes, diagnosis, and treatment
Before beginning any treatment on admission, venous blood was collected in the morning after an overnight fast using an automatic analyzer Vitors to measure the serum concentrations of UA, albumin , fasting glucose, ALT, AST, and blood creatinine in the Clinical Laboratory of the West China Hospital of Sichuan University. In total, patients received lumbar punctures during the acute phase; therefore, the concentrations of cerebrospinal fluid protein CSFP and cerebrospinal fluid glucose CSFG were also determined using the same analyzer. Patients were divided into group with pain and group without pain to compare the differences in the serological and cerebrospinal fluid indexes.
To examine the association between the disability of the GBS patients and pain , Spearman's correlation analysis was performed, and a multiple linear regression was performed to correct for age, gender and history of diabetes.
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The comparisons of the concentrations of UA and albumin between the pain group and the nonpain group were performed using Student's t -tests. The comparisons of the concentrations of CSFP between the pain group and the nonpain group were performed using a rank sum test. A logistic regression was performed to examine the association between pain and the serological and cerebrospinal fluid indexes.
In total, GBS patients were enrolled in this study. The baseline and clinical characteristics of all enrolled patients are shown in Table 1. The male-to-female ratio was approximately 1. Of the patients, 87 In total, 40 of the 87 Radicular pain The characteristics of the 87 patients who reported pain are shown in Table 2.
These data were shown in Table 3. The correlations between the serological and cerebrospinal fluid indexes and the incidence of pain were listed in Table 4. A logistic regression was performed to examine the association between pain and the serological and cerebrospinal fluid indexes Table 5. Previously, the pain component of GBS has hardly got much attention. Multiple reasons may contribute to the lower incidence of pain observed in our study. Firstly, we only included patients within the first 3 weeks of GBS onset, thus, there may have been a loss of some of patients.
Secondly, patients did not reported their pain even though it was present a frequent occurrence when patients did not want to divert the physicians attention from treating the primary disease. Third, the pain assessment methods may be different the pain might not been mentioned by the patient in describing their complaint , and the incidence of pain may differ among the subtypes of GBS.
Finally, pain tolerance may differ among individuals with different ethnicities. In our study, Recently, the relationship between pain and disability in GBS patients has gradually gained attention but remains controversial. In a previous study, no significant correlation was observed between disability and pain intensity. Although the exact reason for this finding was unclear, we hypothesize that the following reasons may be involved.
Secondly, the pathogenesis of GBS may be different in patients with obvious symptoms; and thirdly, pain may serve as a warning signal, leading patients to visit a doctor. After experiencing pain , the patients visited the hospital, which might allow the earlier detection of the disease, timely treatments, and a possible reduction in the proportion of severe GBS patients. This study was the first to report that the incidence of pain is positively correlated with the concentration of CSFP.
The elevated CSFP concentrations would likely stimulate nerve root inflammation and influence afferent sensory nerves, and nerve inflammation could also cause elevated CSFP levels.
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It was a retrospective study that might has some defects in the data collection, statistical errors may have occurred in this study, and further prospective studies with larger sample sizes are required to confirm these results. In addition, we found that the most frequent pain location was the lower limbs, followed by the lower back and back, which was consistent with a previous study. In total, 40 of 87 Radicular pain and muscle pain were the most common types of pain in the GBS patients during the acute phase. Pain in GBS may be attributed to several possible causes.
First, inflamed or damaged large myelinated sensory fibers may lead to dysesthesia and muscle pain in the extremities,  which may account for the lower limbs being the most frequently reported pain location.