Jai Madhok

Stanford University

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Clark G. Owyang

Weill Cornell Medicine

Nitish V. Thakor

Johns Hopkins University

Xiaofeng Jia

University of Maryland, Baltimore

Antonio Loforte

Libera Università Maria SS. Assunta

Mauro Panigada

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico

Su Hwan Lee

Yonsei University

Brigid C. Flynn

University of Kansas

Toshiki Yokoyama

Tosei General Hospital

Davide Chiumello

Azienda Socio Sanitaria Territoriale Santi Paolo e Carlo

Eva Miranda Marwali

National Brain Centre

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University of Oxford

905

Johns Hopkins Hospital

430

Prince Charles Hospital

388

All India Institute of Medical Sciences Rishikesh

387

All India Institute of Medical Sciences Raipur

383

Inserm

276

Assistance Publique – Hôpitaux de Paris

166

Université Paris Cité

123

Stanford University

University of Queensland

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Catecholamine-induced cerebral vasospasm and multifocal infarctions in pheochromocytoma

Endocrinology Diabetes and Metabolism Case Reports (2020)

Jai Madhok Amy Kloosterboer Chitra Venkatasubramanian Frederick G. Mihm

Summary We report the case of a 76-year-old male with a remote history of papillary thyroid cancer who developed severe paroxysmal headaches in the setting of episodic hypertension. Brain imaging revealed multiple lesions, initially of inconclusive etiology, but suspicious for metastatic foci. A search for the primary malignancy revealed an adrenal tumor, and biochemical testing confirmed the diagnosis of a norepinephrine-secreting pheochromocytoma. Serial imaging demonstrated multiple cerebral infarctions of varying ages, evidence of vessel narrowing and irregularities in the anterior and posterior circulations, and hypoperfusion in watershed areas. An exhaustive work-up for other etiologies of stroke including thromboembolic causes or vasculitis was unremarkable. There was resolution of symptoms, absence of new infarctions, and improvement in vessel caliber after adequate alpha-adrenergic receptor blockade for the management of pheochromocytoma. This clinicoradiologic constellation of findings suggested that the etiology of the multiple infarctions was reversible cerebral vasoconstriction syndrome (RCVS). Pheochromocytoma remains a poorly recognized cause of RCVS. Unexplained multifocal cerebral infarctions in the setting of severe hypertension should prompt the consideration of a vasoactive tumor as the driver of cerebrovascular dysfunction. A missed or delayed diagnosis has the potential for serious neurologic morbidity for an otherwise treatable condition. Learning points: The constellation of multifocal watershed cerebral infarctions of uncertain etiology in a patient with malignant hypertension should trigger the consideration of undiagnosed catecholamine secreting tumors, such as pheochromocytomas and paragangliomas. Reversible cerebral vasoconstriction syndrome is a serious but reversible cerebrovascular manifestation of pheochromocytomas that may lead to strokes (ischemic and hemorrhagic), seizures, and cerebral edema. Alpha-adrenergic receptor blockade can reverse cerebral vasoconstriction and prevent further cerebral ischemia and infarctions. Early diagnosis of catecholamine secreting tumors has the potential for reducing neurologic morbidity and mortality in patients presenting with cerebrovascular complications.

Etiology

Stroke

10.1530/edm-20-0078

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Citations (10)

Thrombotic Thrombocytopenic Purpura/Hemolytic Uremic Syndrome and Disseminated Intravascular Coagulation

Cambridge University Press eBooks (2023)

Jai Madhok

Thrombotic microangiopathies (TMA) are a group of conditions characterized by excessive platelet activation, resulting in microvascular thrombi and platelet consumption (thrombocytopenia). The thrombosed microvasculature shears red blood cells (RBCs), causing microangiopathic hemolytic anemia. Primary TMAs include thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS), while secondary TMAs result from infection, pregnancy, malignancy, drugs and toxins, among other causes.

Schistocyte

Microangiopathic hemolytic anemia

Purpura (gastropod)

10.1017/9781009052566.047

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Contents

Journal of Cardiothoracic and Vascular Anesthesia (2022)

Natalie J. Bodmer Vikram Fielding‐Singh Matthew W. Vanneman Andrew Gessouroun Brigid C. Flynn

10.1053/s1053-0770(22)00088-x

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Antithrombin in Extracorporeal Membrane Oxygenation: To Replenish or Not to Replenish?

Critical Care Medicine (2021)

Jai Madhok Stephen J. Ruoss

1 Divsion of Critical Care Medicine and Adult Cardiothoracic Anesthesiology, Department of Anesthesiology, Pain, and Perioperative Medicine, Stanford University School of Medicine, Stanford, CA 2 Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Stanford University School of Medicine, Stanford, CA The authors have disclosed that they do not have any potential conflicts of interest.

Pain medicine

Perioperative medicine

Pulmonary medicine

Respiratory Medicine

10.1097/ccm.0000000000004812

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Hypothermia Amplifies Somatosensory-evoked Potentials in Uninjured Rats

Journal of Neurosurgical Anesthesiology (2012)

Jai Madhok Dan Wu Wei Xiong Romergryko G. Geocadin Xiaofeng Jia

Temperature fluctuations significantly impact neurological injuries in intensive care units. As the benefits of therapeutic hypothermia continue to unfold, many of these discoveries are generated by studies in animal models undergoing experimental procedures under the influence of anesthetics. We studied the effect of induced hypothermia on neural electrophysiological signals of an uninjured brain in a rodent model while under isoflurane. Fourteen rats were divided into 2 groups (n=7 each), on the basis of electrode placement at either frontal-occipital or primary somatosensory cortical locations. Neural signals were recorded during normothermia (T=36.5 to 37.5°C), mild hypothermia (T=32 to 34°C), and hyperthermia (T=38.5 to 39.5°C). The burst-suppression ratio was used to evaluate electroencephalography (EEG), and amplitude-latency analysis was used to assess somatosensory-evoked potentials (SSEPs). Hypothermia was characterized by an increased burst-suppression ratio (mean±SD) of 0.58±0.06 in hypothermia versus 0.16±0.13 in normothermia, P<0.001 in frontal-occipital; and 0.30±0.13 in hypothermia versus 0.04±0.04 in normothermia, P=0.006 in somatosensory. There was potentiation of SSEP (2.89±1.24 times the normothermic baseline in hypothermia, P=0.02) and prolonged peak latency (N10: 10.8±0.4 ms in hypothermia vs. 9.1±0.3 ms in normothermia; P15: 16.2±0.8 ms in hypothermia vs. 13.7±0.6 ms in normothermia; P<0.001), whereas hyperthermia was primarily marked by shorter peak latencies (N10: 8.6±0.2 ms, P15: 12.6±0.4 m; P<0.001). In the absence of brain injury in a rodent model, hypothermia induces significant increase to the SSEP amplitude while increasing SSEP latency. Hypothermia also suppressed EEGs at different regions of the brain by different degrees. The changes to SSEP and EEG are both reversible with subsequent rewarming.

Somatosensory evoked potential

10.1097/ana.0b013e31824ac36c

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Citations (33)

Unexpected Interruptions in the Inhaled Epoprostenol Delivery System: Incidence of Adverse Sequelae and Therapeutic Consequences in Critically Ill Patients

Critical Care Explorations (2021)

Jason M. Block Jai Madhok Clark G. Owyang Kristen Merriman Stephen J. Ruoss

Inhaled epoprostenol is a continuously delivered selective pulmonary vasodilator that is used in patients with refractory hypoxemia, right heart failure, and postcardiac surgery pulmonary hypertension. Published data suggest that inhaled epoprostenol administration via vibrating mesh nebulizer systems may lead to unexpected interruptions in drug delivery. The frequency of these events is unknown. The objective of this study was to describe the incidence and clinical consequences of unexpected interruption in critically ill patients.

10.1097/cce.0000000000000548

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Point-of-Care Ultrasound (POCUS) Predicts Clinical Outcomes in Patients with COVID-19

medRxiv (Cold Spring Harbor Laboratory) (2021)

Andre Kumar Isabel Weng Sally Graglia Thomas Lew Kavita Gandhi

Abstract Introduction Point-of-care ultrasound (POCUS) may detect the cardiopulmonary manifestations of COVID-19 and expediently predict patient outcomes. Methods We conducted a prospective cohort study at four medical centers from 3/2020-1/2021 to evaluate POCUS findings and clinical outcomes with COVID-19. Our inclusion criteria included adult patients hospitalized for COVID-19 who received cardiac or lung POCUS with a 12-zone protocol. Images were interpreted by two reviewers blinded to clinical outcomes. Our primary outcome was ICU admission incidence. Secondary outcomes included intubation and supplemental oxygen usage. Results N=160 patients (N=201 scans) were included. Scans were collected a median 23 hours (IQR:7-80) from emergency department triage. Triage POCUS findings associated with ICU admission included B-lines (OR 4.41 [95% CI:1.71-14.30]; p<0.01) or consolidation (OR 2.49 [95% CI:1.35-4.86]; p<0.01). B-lines were associated with intubation (OR 3.10 [95% CI:1.15-10.27]; p=0.02) and supplemental oxygen usage (OR 3.74 [95% CI:1.63-8.63; p<0.01). Consolidations present on triage were associated with the need for oxygen at discharge (OR 2.16 [95% CI: 1.01-4.70]; p=0.047). A normal lung triage scan was protective for ICU admission (OR 0.28 [95% CI:0.09-0.75; p<0.01) or need for supplemental oxygen during the hospitalization (OR 0.26 [95% CI:0.11-0.61]; p<0.01). Triage cardiac POCUS scans were not associated with any outcomes. Discussion Lung POCUS findings detected early in the hospitalization may provide expedient risk stratification for important COVID-19 clinical outcomes, including ICU admission, intubation, or need for oxygen on discharge. A normal admission scan appears protective against adverse outcomes, which may aid in triage decisions of patients.

Triage

Lung Ultrasound

10.1101/2021.04.13.21255445

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Information theoretical assessment of neural spiking activity with temperature modulation

Annual International Conference of the IEEE Engineering in Medicine and Biology Society (2009)

Jai Madhok Xiaofeng Jia Young-Seok Choi Dandan Zhang Nitish V. Thakor

Previous research has shown that hypothermia immediately after Cardiac Arrest (CA) improves neurological outcomes. In order to study how hypothermia affects neural spiking, cortical and subcortical neural activity was recorded from rodents. Consistent with previous findings, preliminary results show that the firing rate is proportional to the temperature. We also studied the information coded in the spike-timing information of individual neurons and observed that information content varies with temperature. Furthermore, there is an increased dependence between the cortex and sub-cortical structures such as the Thalamus during hypothermia. The latter is most likely an indicator of coupling between these highly connected structures in response to temperature manipulation leading to arousal after global cerebral ischemia.

Modulation (music)

Neural Activity

10.1109/iembs.2009.5334616

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1037: DUAL TRAINING IN ANESTHESIOLOGY AND INTERNAL MEDICINE: SYNERGISTIC PATHWAY TO CRITICAL CARE MEDICINE

Critical Care Medicine (2019)

An La Jai Madhok

Critical Care Medicine: January 2020 - Volume 48 - Issue 1 - p 498 doi: 10.1097/01.ccm.0000643084.89946.f6

Pain medicine

10.1097/01.ccm.0000643084.89946.f6

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