Case Report M. Mouallem, E. Friedman, R. Pauzner, E. Schwartz, E. Rubinstein Rickettsiosis-Associated Hyponatremia Summary: Two patients with hyponatremia (130 mEq/l and 122 mEq/l, respectively), and rickettsial disease are described. The causes of hyponatremia were attributed to rickettsial vasculitis and increased capillary permeability in the first patient and to the syndrome of inappropriate anti-diuretic hormone (ADH) secretion in the second patient. The differentia- tion between the mechanisms was established by measurement of urinary sodium excretion which was low in the first patient (7 mEq/1) and high in the second patient (60 mEq/l), and levels of ADH that were inap- propriately high in the second patient (7-9 pg/ml) in the presence of tow plasma osmolality. The differentia-" tion between these causes of hyponatremia has im- portant therapeutic implications. Zusammenfassung: Hyponatriiimie bei Rickettsiose. Es werden zwei Patienten beschrieben, die bei einer Rik- kettsien-Infektion eine Hyponatri/imie von 130 m,~q/1 bzw. 122 m)kq/1 entwickelten. Die Ursache ffir die Hy- ponatri~imie wird beim ersten Patienten in einer Rik- kettsien-Vaskulitis mit erhrhter Kapillarpermeabilit~it und beim zweiten in einer inad~iquaten Sekretion von antidiuretischem Hormon (ADH) gesehen. Durch Messung der Natriumausscheidung im Urin war eine Differenzierung der beiden Pathomechanismen mrg- lich: beim ersten Patienten war die Natriumausschei- dung mit 7 mJkq/l niedrig und beim zweiten mit 60 m,~q/1 hoch. Zudem waren die ADH-Spiegel beim zweiten Patienten mit 7-9 pg/ml bei geringer Plasma- osmolalit~it unangemessen hoch. Die Unterscheidung der Ursachen der Hyponatri~imie hat wichtige thera- peutische Konsequenzen. Introduction Hyponatremia is frequently encountered in rickettsial dis- ease, affecting some 50% of the patients (1), yet the mechanisms responsible for this electrolyte disturbance are noi fully understood (2). Two patients with rickettsial disease and hyponatremia were observed. In one, inap- propriate antidiuretic hormone secretion (SIADH) was diagnosed and in the other, no specific cause was found. The nature of rickettsiosis-associated hyponatremia and the different therapeutic approaches are illustrated by these two patients. Case Reports Case 1: A 26-year-old male was admitted because of fever and severe headache of three days duration. Four days after onset of Table 1 : Pertinent laboratory results of patients. Urea (mg/100 ml plasma) 25 <10 Creatinine (mg/t00 ml plasma) 1.4 0.8 Na÷ serum/urine (mEq/l) 130/7 122/60 K÷ serum/urine (mEq/1) 4/28 3.4/60 Osmolality serum/urine (mosmol/l) 269/270 251/842 Urine volume (ml/24 h) 1000-1250 1000 Plasma ADH level (pg/ml)* <0.5** 7-9 (normal values): for osmolalityof <275 mosmolh <0.5 pg/ml) * Plasma ADH was measured by radioimmunoassay, as described in (t2); ** Below detectable levels. the disease a rash that started first on the palms and then spread centripetally appeared. Physical examination showed an ob- viously ill patient with diffuse maculo-papular rash. The tempe- rature was 39°C, pulse ll0/min, blood pressure was 120/70 mmHg. The tip of the spleen was palpable. The rest of the phys- ical examination was normal. Notably, no edema, dehydration or evidence of gastrointestinal fluid loss were present. Labora- tory data (shown in Table I) revealed mild hyponatremia. Thy- roxine and cortisol serum levels were within normal limits. Chest x-ray and EEG were normal. The patient was treated with tetracycline 2 g/day, and oral fluid intake was encouraged; it averaged 2.5 to 3 liters/day. On the 5th treatment day the tem- perature resolved and hyponatremia disappeared. Rickettsial fluorescent antibody (FA) tests and Weil-Felix reaction which, on admission, were negative became positive 10 days later; the OX2 in a titer of 1:120 and OX19 in a titer of 1:640. Spotted fever IgM antibodies were detected. Serum level of ADH obtained on the day of maximal hyponatremia was less than 0.5 pg/ml (below detectable level) (Table 1). Case 2: A 16-year-old male was hospitalized because of fever and headache, unaccompanied by nausea or vomiting, of one week's duration. Two weeks prior to admission he worked on a horse ranch. On physical examination, he appeared ill, febrile (38°C) with relative bradycardia (60/min). Blood pressure was 130/60 mmHg. A fine maculo-papular rash was observed on his chest. Mild cervical lymphodenopathy and mild splenomegaly were the only abnormal physical findings. Specifically, there were no signs of dehydration, edema, neurological deficit or abnormal Received: 17 December 1986/Accepted: 20 April 1987 M. Mouallem, M. D., E. Friedman, M. D., R. Pauzner, M. D., E. Schwartz, M. D., Department of Internal Medicine E, Chaim Sheba Medical Center, Tel Hashomer and Sackler School of Medicine, Tel Aviv University, Israel; E. Rubinstein, M. D., Infectious Diseases Unit, Chaim Sheba Medical Center, Tel Hashomer and Sackler School of Medicine, Tel Aviv Uni- versity, Tel Aviv, Israel. Correspondence to: Meir Mouallem, M. D., Department of Internal Medicine E (# 37), Chaim Sheba MedicalCenter, Tel Hashomer 52621, Israel. Infection 15 (1987) Nr. 5 © MMV Medizin Veflag GmbH Mtinchen, Mtinchen 1987 5 / 315