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Diabetic Ketoacidosis Associated with Guillain-Barre Syndromewith CASE REPORT Diabetic Ketoacidosis Associated with Guillain-Barre Syndromewith AutonomicDysfunction Setsuko Fujiwara, Hiroyuki Oshika, Kenzo Motoki, Kenji Kubo*, Yukiaki Ryujin*, Masahiro Shinozaki**, Takuzo Hano*** and Ichiro Nishio*** Abstract Case Report A37-year-old womanwas admitted in a comatosestate, In March 1996, a 37-year-old womanwas admitted to Koyo after exhibiting fever and diarrhea. Diabetic ketoacidosis Hospital in a comatose state after fever, diarrhea and vomiting was diagnosed due to an increased blood glucose level (672 of 1-week duration. Diabetes mellitus was diagnosed in 1990, mg/dl), metabolic addosis, and positive urinary ketone bod- and the patient had taken anti-diabetic drugs for five years, but ies. On the fifth hospital day, despite recovery from the criti- follow-up was discontinued in 1995. She had no episodes of cal state of ketoacidosis, the patient suffered from dyspha- neurological deficit or fainting and was workingas a nurse. gia, hypesthesia and motor weakness, followed by respira- On admission, Kussmaul's breathing, blood pressure of 96/ tory failure. Cerebrospinal fluid analysis was suggestive of 56 mmHg,and a heart rate of 122/min were observed. DKA Guillain-Barre syndrome (GBS). Autonomic dysfunction was diagnosed on the basis of an increased blood glucose level was manifested as tachycardia and mild hypertension in (672 mg/dl), severe metabolic acidosis (arterial blood gas analy- the acute stage. Marked orthostatic hypotension persisted sis: pH 6.703, PCO2 13.8 mmHg, PO2 281.4 mmHg, HCO3 1.7 long after paresis was improved, indicating an atypical clini- jjmol//, BE -36.3 jimol//) and urinary ketone bodies. Other labo- cal course of GBS. ratory findings were an electrolyte imbalance (Na 156.0 mEq//, (Internal Medicine 39: 495-498, 2000) K 1.67 mEq//), leucocytosis of 17,600/mm3 and an elevated C- reactive protein level of 2. 1 mg/dl. Serum ketone bodies (22,740 Keywords: acute polyneuropathy, diabetes mellitus, ortho- jimol//) and the hemoglobin A1C level (14.0%) were increased. static hypotension Thyroid function was within normal and autoantibodies were not detectable. The electrocardiogram revealed sinus tachycar- dia and significant QT prolongation, although the chest X-ray and echocardiogram findings were normal. Introduction After treatment with insulin, hypotonic saline infusion and artificial ventilation for 15 hours, consciousness was regained Guillain-Barre syndrome (GBS) is rapidly progressive and and the ketoacidosis gradually improved. On the fourth hospi- is reversible in manycases, but sometimes causes fatal tal day, neurological abnormalities were not observed, and the polyradiculoneuropathymanifesting as muscleweaknessand results of the blood gas analysis and the electrolyte levels had respiratory failure (1, 2). improved. Signs of autonomic involvement, such as tachycardia, ar- On the sixth day, the patient suddenly complained of dys- rhythmia, hypertension, orthostatic hypotension, abnormal phagia, paresthesia, hypesthesia and muscle weakness. Oncra- sweating and pupillary and sphincteric dysfunction have been nial nerve examination, the pharyngeal reflex could not be elic- recognized as complications of GBS(3-9). However, most of ited and swallowing was impaired. The lower extremities were these dysautonomias are detected in the early stage of GBS(6, more severely involved than the upper extremities, and the legs 7). were paralyzed. Muscle strength in the upper limbs was rated Wereport here a patient with GBSfollowing diabetic ke- as 3 by manual muscle testing, there was no ataxia, and the toacidosis (DKA), in whommarked autonomic dysfunction deep tendon reflexes were absent. Paresthesia was present in including orthostatic hypotension and paralytic mydriasis per- all four extremities, in the trunk and in the face; in addition, sisted after remission of motor paresis. glove-and-stocking-type pain and temperature disturbances, and From the Department of Cardiology, Koyo Hospital, Wakayama,*the Department of Neurosurgery, Koyo Hospital, Wakayama,* *the Critical Care Medical Center, WakayamaMedical College, Wakayamaand ***the Division of Cardiology, Internal Medicine, WakayamaMedical College, Wakayama Received for publication February 17, 1998; Accepted for publication January 20, 2000 Reprint requests should be addressed to Dr. Setsuko Fujiwara, the Department of Cardiology, Koyo Hospital, 40 Tsuhata, Wakayama, Wakayama640-83 15 Internal Medicine Vol. 39, No. 6 (June 2000) 495 Fujiwara et al diminished vibration sense in the legs were observed. Mild 144 mg/dl). hypertension, sinus tachycardia (HR: 136/min) and sweating The patient recovered from the respiratory failure in three were recognized. Twenty hours later, respiratory failure oc- weeks, whenshe complained of photophobia. Mydriasis and curred, necessitating artificial ventilation (Fig. 1). Since GBS loss of the pupillary light reflex, abrupt sweating and sphinc- was suspected by the results of the cerebrospinal fluid (CSF) teric dysfunction werealso observed. examination (protein 1 84 mg/dl, 2 mononuclear leukocytes/ After three months, remission of motor paresis was obtained. mm3), high-dose y-globulin (Venilon® 500 mg/kg/day) was ad- However, frequent syncope in the sitting position caused the ministered for five days. patient still to be bedridden. To evaluate autonomic nerve func- The patient was transferred to Critical Care Medical Center tion, weperformed several tests by direct blood pressure mea- (CCMC)of WakayamaMedical College and managed there surement (Fig. 2). In the 30° head-up tilt test, systolic blood for the next 20 days. Onthe third day of the polyneuropathy, pressure immediately decreased below 50 mmHg,and heart motor nerve conduction velocities (MNCVs)measured in the rate did not increase. OnValsalva's maneuver, no heart rate ulnar nerves (right 40.3, left 43.4) were slow (normal range increase in phase II or over-shooting of blood pressure in phase 55.1±6.4 m/sec), while those in the tibial nerves (right 40.6, IV was observed. During the cold pressor test, neither heart left 45.0) were almost normal (normal range 50.2±9.3 m/sec). rate nor blood pressure increased. In myocardial scintigraphy However, the thresholds of stimulation were increased above using 123I-metaiodobenzylguanidine (MIBG) (10, 1 1), which 95 mAeven in the tibial nerves. On the 19th day, the second showscardiac adrenergic innervation, myocardial MIBGup- examination revealed improvementin the thresholds and de- take was barely observed (heart/background ratio: 1.62). lay in MNCVs(right ulnar nerve 43.1, left 45.7, right tibial The dysphagia improved in about four months. Six months nerve 31.5, left 35.9 m/sec) with temporal dispersion in the after admission, the patient becamesyncope-free and wasdis- left upper limb. Conduction block was not observed in these charged. Repeat of the 30° head-up tilt test revealed a decrease tests. Repeated CSFanalysis revealed no leukocytes, but pro- in systolic blood pressure to 74 mmHg,showing slight im- tein levels were still elevated on the fifth and 19th days (141, provement of the postural hypotension. Sinus tachycardia Admissi on Discharge ^1996 ICCMC 1 Jr 1997 Mar Apr [May]Jim[July[Aug|Sep[ Oct|Nov tMay Aft ~12 I13I14»15I16I17f18'19" ''IP 9 '' " 1 lull - 60- ^r^ O 0 F^ - // If- ^ __ jf^^tM^^^^^ Dysphagia ^^^^^^^^^^y fcggggSgllSy ^g^^^^M Paresis (upper < lower) ^^^^^^j^ Insulm I 4-. «-rt ostatic ypotension g:;:;:;:;:;:;;;:;:;:;;^^^;-^^^ C2ESS3 I InfusionV *å » [jjllgijgi Carbamazepine 100 mg ] |NaHCO3| B^^iobS^ roigg^ji Midodrine4 mg ; ' | f^H [."kcTs I 1 ^à"l--.;--.r-;-^ |' Carteolol10mg j I I Figure 1. Clinical Course. CCMC:Critical Care Medical Center, WakayamaMedical College. SBP: systolic blood pressure (A).(å supine position, å¡ sitting position). DBP: diastolic blood pressure (à" supine position, O sitting position). HR: heart rate 496 Internal Medicine Vol. 39, No. 6 (June 2000) Guillain-Barre Syndrome and Dysautonomia 30° head-up tilt test u1501 å à"- ~ : = '-- £PQ so-o-" HR104/min - .._ W^«^*a^. 106/min mumm^ Valsalva's maneuver g150n-----,. - , --;- « 50- . å '- ^%4JWWMf|JW^^ W 0J ^HR100/min"~ - "à" 106/min1-'--, "' ^ Cold pressor test ^B 50- -,- à" ' - - gj J HR102/min - 102/min Figure 2. Records of direct blood pressure in the 30° head-up tilt test, Valsalva's ma- neuver and cold pressor test (July 1996). BP: blood pressure. HR: heart rate. gradually improved over one year. the CSFprotein level was within the normal range and diffuse By two years after the onset of symptoms, the patient had axonal degeneration was demonstrated in a sural nerve biopsy. completely recovered from the motor paresis and loss of sen- The paresis in that case never completely remitted. In the present sation, except for vibration sense. Deeptendon reflexes in the case of neuritis, acute axonal degeneration could not be com- lower extremities continued to be weak. Although subclinical pletely ruled out without a nerve biopsy. orthostatic hypotension and a mild form of paralytic mydriasis Manypatients with GBSdescribe preceding minor events, persisted, I23I-MIBG myocardial scintigram revealed restora- most of which are viral infections, and association of GBSwith tion of radioactivity in the antero-lateral wall and interventricu- preceding surgery, vaccination and malignancy has also been lar septum. reported (1, 15). Recently, the importance of the severe form of acute polyneuropathy in critically ill patients has been re- Discussion ported. This condition develops immediately after sepsis,
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