the medical casualty

Upon arrival to the medical casualty, the patient CNS examination revealed a power of 2-3/5both sides with areflexia and hypotonia. He also had loss of sensation on his palm and soles of his feet. Patient was admitted to the medical ward and he developed inability to breath and he desaturated 82-88 % on 6l o2. He was then intubated and connected to a ventilator and was admitted to the ICU. Upon admission to the ICU he was mechanically ventilated. His CXR, LFT, BUN/CR, platelets , coagulation profile , WBC( but neutrophil 86%) were normal. He was afebrile. His ETT secretion showed cocci +++ and bacilli++. ECG showed SR and evidence of autonomic dysfunction supporting GBS. During the ICU stay the patient was assessed daily regarding his motor and bulbar affection which showed gradual improvement. He was on minimal heparin for DVT prophylaxis. The patient received his IVIG for 5 days. The patient was extubated and he is able to drink and swallow. He had a delusional state and the psychiatric was consulted and said that this was illogical overvalued idea not reaching the delusional state; he was given haloperidol 1.25 mg BD. The patient developed fever and was on rocephin and klacid by the third day. He then had staph aures pnemoniatis and klacid was changed to tazocin for 7 days. The patient developed thrombocytpenia , may be due the zintac,? and combined hepatocellular and cholestatic liver impairment, may be due to antibiotics?. The patient was investigation for the lymphopenia ; he is HIV,HB ,HC negative . The patient was transferred back to the medical ward and showed gradual improvement in his motor function. But he started to develop severe pain that is affecting his sleep. He also had photophobia and constipation. He is now feeling better and able to sleep and swallow and he pain reduced to some extent. He does not have numbness.

The most recent blood investigation: in 5/1/2010

  • Clinical chemistry:
  • Glucose : 4.8(normal)
  • BUN : 3.7(normal)
  • Creatinine 60 (normal)
  • Sodium: 139 (normal)
  • Potassium: 4.1 ( normal)
  • Chloride103 (normal)
  • Calcium; 2.3( normal)
  • Phos: 1.52(high)
  • MG: 0.9(normal)
  • ALB: 32 ( low)
  • Anion gap: 11.1(normal)
  • ?Hematology :
  • Hb: 111(low)
  • WBC: 8.2(normal)
  • RBC: 4.5(normal)
  • Hematocrit: 0.33 (low)
  • MCV: 73 (low)
  • MCHC: 336(normal)
  • RDW:12.7(high)
  • Platelets:260( normal)
  • MPV: 8.3 (normal)
  • WBC diff:
  • ?Neutrophils: 0.6
  • ?Lymphocyte:o.25
  • ?Monocyte: 0.09
  • ?Basophils: 0.0
  • )
  • Coagulation profile is normal

20 yrs old Kuwaiti male with a history of alopecia universalis, diarrhea, and recent vaccination for HBV presented with 2 days history of numbness and rapidly progressive muscle weakness that started in his lower limbs distal to proximal and then ascended to evolve his upper limbs. He also developed difficulty in breathing, speech, loss of sphincteric control?. As for his investigation, CXR, CT, LP, urine R/M showed no detected abnormality. His SUE, CBC, Coagulation profile showed no relevant abnormality. Subsequent ECG showed some element of autonomic dysfunction. He is HBV, HIV, HCV negative. His NCS showed diffuse motor neuropathy consistent with ADIP variant of GBS ( Guillian barre syndrome). The patient was diagnosed with GBS. GBS is an acute, frequently severe and fulminant polyradiculoneuropathy and considered to be a heterogeneous grouping of immune-mediated processes characterized by motor, sensory, and autonomic dysfunction. Males are 1.5 times more likely to get GBS and the disease has bimodal distribution with a peak during young adulthood (15-35 yrs); these could be possible risk factors for this patient to have the disease. The clinical features of GBS include rapidly progressive a/hyporeflexic symmetric ascending muscle weakness with or without sensory disturbances. The weakness usually evolves over hours to days accompanied with tingling sensation in the extremities. The lower cranial nerves can be involved causing bulbar weakness and difficulty handling secretion and maintaining the airway. The patient can experience severe pain even on the slightest movements. Loss of vibration, proprioception, touch, and pain distally may be present. Bladder dysfunction may also occur. Autonomic dysfunction is not uncommon. Additionally, constipation due to bowel paresis and gastric dysmotility may be experienced. This patient had most of the above mentioned symptoms. Several subtypes of GBS have been recognized. These include the acute inflammatory demyelinating polyneuropathy (AIDP) which is generally preceded by a bacterial or viral infection. This patient had this type. It also includes the acute motor axonal neuropathy (AMAN) which is purely motor, acute motor-sensory axonal neuropathy (AMSAN) that afflicts sensory nerves and roots and Miller-Fisher syndrome (MFS) that has triad of ataxia, areflexia, and ophthalmoplegia. Other regional variants have been also identified. GBS is believed to result from autoimmune humoral- and cell-mediated responses to a recent infection as well as recent vaccination. Its relation to antecedent infections suggests that molecular mimicry may be a possible mechanism. Antibodies formed against ganglioside-like epitopes in the lipopolysaccharide (LPS) layer of some infectious agents have found to cross-react with the ganglioside surface molecules of peripheral nerves. The (AIDP) subtype is generally preceded by a bacterial or viral infection. Nearly 40% of patients are seropositive for Campylobacter jejuni. Symptoms generally resolve with remyelination. The fact that this patient had a history of diarrhea and recent vaccination may explain his condition. As for the work up, the Diagnosis of Guillain-Barr? syndrome usually is made on clinical grounds. Laboratory studies are useful to rule out other diagnoses and to better assess functional status and prognosis. The treatment of choice of GBS includes IVIG for 5 days or plasmapheresis. Although both are equally effective, IVIG is easier to administer and has fewer complications than plasma exchange. A combination of the two therapies is not significantly better than either alone. In the worsening phases of the disease, most patients should be monitored in critical care setting.

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