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Guillain–Barré syndrome after acute myocardial infarction: A rare presentation
 

Guillain–Barré syndrome after acute myocardial infarction: A rare presentation

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The association of acute coronary syndrome with any immunological mediated polyradiculopathy like Guillain–Barré syndrome is very rare. We report such a rare association of acute myocardial ...

The association of acute coronary syndrome with any immunological mediated polyradiculopathy like Guillain–Barré syndrome is very rare. We report such a rare association of acute myocardial infarction and Guillain–Barré syndrome. Our patient underwent primary angioplasty successfully, but developed respiratory failure while in hospital. While the difficulty in weaning off from ventilator a suspicion of neuromuscular disease was made. The further investigations, including nerve conduction study confirmed a diagnosis of Guillain–Barré syndrome. Despite treatment, the patient died secondary to multi-organ dysfunction. Our case is 4th reported in the literature without use of any thrombolytic agent for such association.

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    Guillain–Barré syndrome after acute myocardial infarction: A rare presentation Guillain–Barré syndrome after acute myocardial infarction: A rare presentation Document Transcript

    •                                                                                                   Guilla                                      ain-Barre infar        e syndro rction: A ome afte rare pre    r acute m esentatio myocard on  ial
    • Case Report GuillaineBarre syndrome after acute myocardial infarction: A rare presentation Pankaj Jariwala a,* , Harikishan Boorugu b , Gopal Chevuru c , Arshad Punjani b , Shaeq Mirza b , Dilip Babu Madhawar d , Nikhilkumar Kotla e , Srinivasrao Bopparaju f a Consultant Cardiologist, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, India b Consultant Physician, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, India c Consultant Neurologist, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, India d Consultant Nephrologist, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, India e Medical Registrar, Apollo Hospitals, Near Old MLA Quarters, Hyderabad, AP, 500095, India f Consultant Nephrologist, Matrix Hospital, Ramanthapur, Hyderabad, AP, 500013, India a r t i c l e i n f o Article history: Received 11 February 2014 Accepted 1 May 2014 Available online xxx Keywords: GuillaineBarre syndrome Acute myocardial infarction Primary percutaneous angioplasty a b s t r a c t The association of acute coronary syndrome with any immunological mediated poly- radiculopathy like GuillaineBarre syndrome is very rare. We report such a rare association of acute myocardial infarction and GuillaineBarre syndrome. Our patient underwent pri- mary angioplasty successfully, but developed respiratory failure while in hospital. While the difficulty in weaning off from ventilator a suspicion of neuromuscular disease was made. The further investigations, including nerve conduction study confirmed a diagnosis of GuillaineBarre syndrome. Despite treatment, the patient died secondary to multi-organ dysfunction. Our case is 4th reported in the literature without use of any thrombolytic agent for such association. Copyright © 2014, Indraprastha Medical Corporation Ltd. All rights reserved. 1. Introduction GuillaineBarre syndrome and its association with cardiovas- cular diseases are rare. There are a few case reports of auto- nomic dysfunction leading to the manifestation of cardiac dysfunction in the form of transient variant of Tako-Tsubo cardiomyopathy,1 STeT changes in the form of giant T wave inversions2 and ST elevations with normal coronaries3 in the literature. There are few case reports in the literature of rare as- sociation of development of GuillaineBarre syndrome following acute myocardial infarction.4,5 Whether this is mere (part of the association) coincidence or neurological manifestation secondary to myocardial infarction needs to be established. We report such a case of acute myocardial infarction with cardiogenic shock with acute left ventricular failure who could not be weaned off ventilator and subsequently diagnosed to have the GuillaineBarre syndrome, which despite management could not * Corresponding author. Tel.: þ91 9393178738. E-mail address: pankaj_jariwala@hotmail.com (P. Jariwala). Available online at www.sciencedirect.com ScienceDirect journal homepage: www.elsevier.com/locate/apme a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e5 Please cite this article in press as: Jariwala P, et al., GuillaineBarre syndrome after acute myocardial infarction: A rare pre- sentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2014.05.009 http://dx.doi.org/10.1016/j.apme.2014.05.009 0976-0016/Copyright © 2014, Indraprastha Medical Corporation Ltd. All rights reserved.
    • survive secondary to respiratory and kidney failure leading to death. 2. Case report A 56 years old male arrived at an emergency room of a pe- ripheral non-PCI hospital with complaints of retrosternal chest pain for 6 h associated with diaphoresis and breath- lessness at rest. On examination, he had tachypnea and he was restless with heart rate of 40 per min and blood pressure recorded in the left upper extremity was 80/60 mm Hg and respiratory rate was 42 per minute. His right upper limb had post-polio re- sidual paralysis with wasting and atrophic changes. There were no cyanosis and edema. On Cardio-respiratory examination, though he had normal heart sounds without any murmurs, but there were bilateral basal crackles in less than 50% of the lungs. Nervous system examination revealed normal higher functions and patient was moving all limbs well, except the polio affected right upper limb (which had power of 3/5). The ECG showed an acute ST elevation in the inferior leads and V1 with reciprocal ST depression in Antero-lateral leads [Fig. 1a]. Cardiac rhythm showed AV dissociation. Hence, clinical diagnosis of inferior wall myocardial infarction [STEMI] with complete heart block with Cardio- genic Shock was made. Bedside 2 D echocardiography showed hypokinesia of inferior wall and posterior wall with hyper contractile other segments with ejection fraction of 35%. There was no mitral regurgitation or ventricular septal defect [Mechanical complication]. The patient was shifted to PCI hospital where on arrival patient was in normal sinus rhythm and shifted to the Cath lab after initial stabilization. Coronary angiography revealed osteal chronic total occlusion of left anterior descending artery with normal left circumflex and OM arteries. RCA injection showed thrombotic total oc- clusion of the mid segment [TIMI 0]. Primary PCI of RCA done after thrombo-aspiration with implantation of BMS, which restored TIMI 3 flow [Door to needle time e 94 min]. [Fig. 2aef] Post angioplasty ECG showed >75% resolution of ST elevations in the inferior leads and reciprocal ST de- pressions in Antero-lateral leads with normal sinus rhythm [Fig. 1b]. Immediately after primary PCI patient developed in- crease in breathlessness with a further drop in oxygen saturation hence he was ventilated by inserting an endotracheal tube and shifted to cardiac ICU intensive care unit. The Patient required high doses of inotropes, blood pressure which did not improve hence IABP was inserted through the right femoral artery for hemodynamic stability. On a ventilator, he had spikes of fever, hence blood culture Fig. 1 e Electrocardiogram pre and post primary percutaneous angioplasty. 1a: Electrocardiogram shows ST elevation of leads II, III, AVF with reciprocal ST depression with complete heart block. 1b: Post primary angioplasty ECG shows >75% resolution of ST elevation and reciprocal ST depression with normal Sinus rhythm. a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e52 Please cite this article in press as: Jariwala P, et al., GuillaineBarre syndrome after acute myocardial infarction: A rare pre- sentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2014.05.009
    • and endotracheal tube cultures were sent and initiated on Meropenem. Despite these efforts his respiratory failure did not improve hence on the 7th day percutaneous tracheos- tomy was done under local anesthesia and ventilation continued through a tracheotomy. Supportive measures in the form of total parental nutrition, antibiotics, respira- tory physiotherapy initiated to improve his respiratory efforts. Fig. 2 e Stepwise procedure of primary percutaneous coronary intervention of the RCA. a, b: Angiography of the left coronary system showing chronic total occlusion of the LAD in LAO cranial and caudal views (arrows). c: angiography of the RCA showing acute thrombotic occlusion (thick arrow) in its mid segment. d: establishment of flow in the RCA with the passage of guide wire across the occlusion with translucency (thick arrow) suggestive of acute thrombus. e: thrombo- aspiration using Export catheter. f: Final angiography after placement of stent showing TIMI 3 flow. Fig. 3 e Nerve conduction study shows the grossly reduced CMAP amplitudes with normal with normal conduction velocities suggestive of axonal motor neuropathy. a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e5 3 Please cite this article in press as: Jariwala P, et al., GuillaineBarre syndrome after acute myocardial infarction: A rare pre- sentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2014.05.009
    • The detailed neurological examination was repeated at this point in view of persisting poor respiratory effort. The patient was found to have areflexic quadriparesis with a power of 1/5 in all limbs (including polio affected limb) along with poor chest expansion suggesting a diffuse neuromuscular illness. His plantars were flexors. Nerve conduction studies of all four limbs revealed grossly reduced CMAP (compound muscle ac- tion potential) amplitudes with normal SNAPs (sensory nerve action potentials). F waves were completely absent. In view of acute onset off quadriparesis, and areflexia with respiratory involvement, nerve conduction suggestive of axonal motor polyradiculoneuropathy, diagnosis of AMAN (acute motor axonal polyradiculoneuropathy) variant of GuillianeBarre syndrome was made [Figs. 3 and 4]. Lumbar puncture could not be done as the patient was on anti-platelet and antico- agulant therapy. A computed tomogram of the brain was normal. Intravenous immunoglobulin could not be given due to cost constraints. Methyl Prednisolone therapy was started, but despite these efforts, patient conditions deteriorated and the patient expired after 2 weeks secondary to sepsis and respiratory failure. 3. Discussion The GuillaineBarre syndrome is an immune mediated acute inflammatory polyneuropathy (predominantly demyelinating type) and it has been reported to be associated with viral in- fections, lupus erythematous, lymphoma, Hodgkin's disease and other situations.6 Differential diagnoses for acute onset quadriparesis in our patient include GuillaineBarre syndrome, hypokalemia, acute transverse myelopathy and acute polyneuropathy secondary to critical illness, etc. His serum potassium was normal, his plantars were down going and absence of F waves and the absence of proximal deep tendon reflexes differentiates it from critical illness neuropathy. A possibility of acute Fig. 4 e Shows normal sensory conduction studies. Table 1 e Summery of case reports of development of GuillaineBarre syndrome after Acute myocardial infarction in literature. Sr. No. Author & Year of publication Age/sex Window period Clinical presentation Diagnosis Recovery Acute coronary syndrome Neurological symptoms 1 McDonough & Dawson4 1987 46 years/male 17 days Acute inferior wall myocardial infarction Generalized weakness of arms and legs. LP & NCV After 2 months with physiotherapy. 65 years/Female 1 week Acute anterior myocardial infarction. Lethargy and paresthesia in the distal arms and legs LP & NCV After 3 months with physiotherapy. 2 M. Sharma et al7 2002 46 years/Male 6 days Acute evolved Antero-lateral myocardial infarction. Paresthesias and weakness of both legs and arms LP & NCV After 30 days with plasmapheresis. a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e54 Please cite this article in press as: Jariwala P, et al., GuillaineBarre syndrome after acute myocardial infarction: A rare pre- sentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2014.05.009
    • infectious spinal arachnoiditis can be considered but sym- metric and diffuse absence of deep tendon reflexes negates the diagnosis of spinal arachnoiditis.7 GuillaineBarre syndrome complicating acute myocardial infarction is a very rare occurrence and till now in literature we could find only two case reports with three cases reported so far as summarized in Table 1.4,5,8 There are case reports of development of GB syndrome following administration of thrombolytic therapy like strep- tokinase, anisostraplase.9e12 But in our case, the patient underwent Primary PCI hence there was no drug attributable to this neurological disease particularly drugs causing peripheral neuropathy. There are certain causative factors in these patients like secondary to respiratory tract infection or certain cardiac drugs like carni- tor which was used in this case. 4. Conclusion We suggest that any patient who complains of generalized weakness or difficulties in weaning off ventilator in cardiac patients should undergo thorough neurological examination and possibility of GB syndrome complicating myocardial infarction should be considered as one the differential di- agnoses. Occurrence of GBS after myocardial infarction is rare and if more cases are reported, will need to look into associ- ation of both. Conflicts of interest All authors have none to declare. r e f e r e n c e s 1. Guglin M, Novotorova I. Neurogenic stunned myocardium and takotsubo cardiomyopathy are the same syndrome: a pooled analysis. Congest Heart Failure (Greenwich, Conn). 2011;17(3):127e132. 2. Yoshii F, Kozuma R, Haida M, et al. Giant negative T waves in GuillaineBarre syndrome. Acta Neurol Scand. 2000 Mar;101(3):212e215. 3. Dagres N, Haude M, Baumgart D, Sack S, Erbel R. Assessment of coronary morphology and flow in a patient with GuillaineBarre syndrome and ST-segment elevation. Clin Cardiol. 2001 Mar;24(3):260e263. 4. McDonagh AJ, Dawson J. GuillaineBarre syndrome after myocardial infarction. Br Med J (Clin Res Ed). 1987 Mar 7;294(6572):613e614. 5. Ng E, Stafford PJ. GuillaineBarre syndrome after myocardial infarction. Int J Cardiol. 2003 Jul;90(1):129e130. 6. Hartung H, Willison HJ, K B. Acute immuno-inflammatory neuropathy: update on GuillaineBarre syndrome. Curr Opin Neurol. 2002;15:571e577. 7. Huynh W, Kiernan MC. Nerve conduction studies. Aust Fam Physician. 2011 Sep;40(9):693e697. 8. Sharma M, Kes P, Basi-Kes V, et al. GuillaineBarre syndrome in a patient suffering acute myocardial infarction. Acta Clinica Croatica. 2002;41(3):255e257. 9. Okuyan E, Cakar MA, Dinckal MH. GuillaineBarre syndrome after thrombolysis with streptokinase. Cardiology Res Pract. 2010 Jan;2010:315856. 10. Eshraghian A, Eshraghian H, Aghasadeghi K. GuillaineBarre syndrome after streptokinase therapy for acute myocardial infarction. Intern Med. 2010;49(22):2445e2446. 11. Patras NK. GuillaineBarre syndrome after treatment with streptokinase. BMJ. 1992;304(May):1992. 12. Kaiser R, Kaufmann R, Czygan M, et al. GuillaineBarre syndrome following streptokinase therapy. Clin Investig. 1993 Oct;71(10):795e801. a p o l l o m e d i c i n e x x x ( 2 0 1 4 ) 1 e5 5 Please cite this article in press as: Jariwala P, et al., GuillaineBarre syndrome after acute myocardial infarction: A rare pre- sentation, Apollo Medicine (2014), http://dx.doi.org/10.1016/j.apme.2014.05.009
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