He presented on the day of hospital admission with severe acute respiratory failure associated with chest X-ray abnormalities but with severe dyspnoea and confusion
He presented on the day of hospital admission with severe acute respiratory failure associated with chest X-ray abnormalities but with severe dyspnoea and confusion. His central body temperature was 38C, arterial blood pressure was 150/90?mm?Hg, pulse rate was 150?bpm, breath rate was 45 breaths/min, pulse oximetry indicated an oxygen saturation value of 85% despite oxygen flow rate set at 15?L/min using a reservoir mask. arterial hypertension. He worked as a horse keeper in a farm. The patient presented 3?days before hospital admission with an acute viral-like illness manifested by fever, diffuse myalgia and generalised weakness. He offered on the day of hospital admission with severe acute respiratory failure associated with chest X-ray abnormalities but with severe dyspnoea and confusion. His central body temperature was 38C, arterial blood pressure was 150/90?mm?Hg, pulse rate was 150?bpm, breath rate was 45 breaths/min, pulse oximetry indicated an oxygen saturation value of 85% despite oxygen flow rate set at 15?L/min using a reservoir mask. Urine output was 400?mL/day. A pulmonary examination showed little bilateral diffuse fine crackles. The cardiovascular examination showed quick and regular heart rate. Livedo was noted on both legs. No skin eruption was noted. Because of the severe acute respiratory failure respiratory support with mechanical ventilation was instaured shortly after admission. Arterial blood pressure fell rapidly to 75/40?mm?Hg. Investigations In ICU and after mechanical ventilation arterial blood gases under FIO2 1 showed: pH ISGF3G 7.19, PaO2 76?mm?Hg, PaCO2 65?mm?Hg, base extra?11, SaO2 88%. White cell count was normal with initial value of 10?000?mm3 but it reached IITZ-01 23?000?mm3 the next day. The patient showed acute renal failure with a serum creatine value of 160?mol/L. Blood chemistry showed no liver function abnormalities but rhabdomyolysis was obvious as creatine kinase level was 1200?UI/L (normal value 250). There was no biological evidence of coagulopathy. Chest X-rays (physique 1) showed moderate bilateral alveolar lung opacities especially in the upper lung fields. Open in a separate window Physique?1 Chest X-rays following mechanical ventilation. Note bilateral alveolar and interstitial opacities especially in the upper fields. Our team relied upon lung ultrasound in the management of acute respiratory failure. The patient’s lung ultrasound showed large bilateral retrodiaphragmatic lung hepatisation associated with diffuse bilateral anterior pulmonary oedema consistent with adult respiratory distress syndrome (ARDS). Right-sided bronchoscopy showed haemorragic secretions and bronchoalveolar lavage showed numerous gram positive cocci which were then identified as subsp. (100?000?cfu/mL). Blood and urine cultures remained unfavorable. Pneumococcal and legionnella urinary soluble antigens were negative. No other pathogen was recognized in the initial bronchoalveolar lavage specimen. Right heart catheter showed high cardiac output failure consistent with septic shock. Pulmonary artery occlusion pressure was 8?mm?Hg, pulmonary artery pressure was 40/25?mm?Hg. Treatment Initial treatment included respiratory support by adequate mechanical ventilation and haemodynamic support using norepinephrine in conjunction with antibiotic treatment by linezolid which was then switched to ceftriaxone and clindamycin for 10?days. Once bacterial identification was made, we added on the second day of admission a dose of 2?g/kg of human polyvalent immunoglobulins and we used high-volume venovenous haemofiltration because the patient developed severe multiorgan failure. End result and follow-up The patient had a good response to initial treatment strategy and recovered within 42?days. IITZ-01 He had severe residual neuromyopathy which needed 2?months of rehabilitation. He returned home and is doing well 6?months after discharge. Conversation To our knowledge only one fatal case of harmful shock syndrome related to subsp was reported.5 The gain of superantigens by subsp has been recently documented and is associated with increased virulence.6 Although earlier reports of human infection of subsp have been made more than 30?years ago,7 this human pathogen seems to be an extremely rare cause of toxic shock syndrome. Only one fatal case of harmful shock IITZ-01 syndrome has been linked to superantigen production by this agent.5 Our patient fulfilled clinical and microbiological criteria for Streptococcal toxic shock syndrome according to the established criteria.8 Treatment strategy was based on.