Chapters authored
Acute Pain Management in Intensive Care Patients: Facts and Figures By Nissar Shaikh, Saher Tahseen, Qazi Zeesan Ul Haq, Gamal Al-Ameri,
Adel Ganaw, Arshed Chanda, Muhammed Zubair Labathkhan and
Tariq Kazi
Pain is an unpleasant experience for all patients including intensive care patients; if it is not treated properly, it has deleterious effects on patients’ acute and chronic well-beings. In ICU patients, it causes sympathetic stimulation leading to adverse hemodynamic effects and after discharge, these patients are at the higher risk for developing chronic pain and post-traumatic stress disorders. Apart from racial and regional factors, sleep deprivation, anxiety, and delirium increase the pain perceptions. Pain assessment is a prerequisite for adequate pain management. The ICU patients are sedated and ventilated, and assessment scales differ depending on whether the patient is able to communicate. There are different pain assessment scales for both groups of patients. The preferred mode of delivery of analgesic medication is intravenous route as intramuscular and subcutaneous route are not reliable for drug delivery in these patients. Patient and nurse controlled analgesia gives better sense of pain control. In the treatment of pain, opioids are the commonly used medications, but paracetamol, dexmedetomidine, and gabapentin are increasingly used. Newer trends are multimodal analgesia, where the combinations of analgesic medications with different mechanism of action are used. Another trend is increasing use of analgosedation; they not only control the pain but also relieve anxiety.
Part of the book: Pain Management in Special Circumstances
Urosepsis: Flow is Life By Nissar Shaikh, Umm-E-Amara, Jazib Hassan, Zeeshan Qazi, Arshad Chanda, Zia Mahemood, Mahommad Zubair, AR Raju Vegensa, Abdul Gafoor M. Tharayil, Adel Ganaw, Ranjan Matthias and Muna Al Musalmani
Urosepsis is one of the important etiological factors for community as well as hospital-acquired infections. Accordingly, urosepsis is divided into community-acquired and hospital-acquired urosepsis. Obstruction to the flow of urine is a common risk factor for community-acquired urosepsis, whereas the indwelling urinary catheter is the risk for the hospital-acquired urosepsis. E. coli remained the most common bacteria-causing urosepsis. If not treated early and appropriately, urosepsis can complicate into septic shock and multiple organ dysfunction. The cornerstone for the improved outcome of these patients is initial resuscitation and proper antibiotic therapy and restoring the flow of urine or removing the infected urinary catheter. Community-acquired urosepsis can be prevented by removing the obstruction to flow of urine permanently. The hospital-acquired urosepsis can be prevented by strictly following catheter-associated urinary tract infection prevention bundle and removing the catheter as early as possible.
Part of the book: Clinical Management of Shock
Peripartum Pulmonary Embolism By Nissar Shaikh, Firdous Ummunnisa, Arshad Chanda, Umm-e-Amara, Mohammed A. Imran, Mahammad Zubair, Jazib Hassan, Mohammad Nayeemmuddin, Qazi Zeeshan, Zia Mahmood, Saher Thaseen, Abdul Gafoor Tharayil, Ranjan Mathias, A.R. Raju Vegesna and Umaiz Momin
Pregnancy and peripartum increase the risk of venous thromboembolism (VTE) by many folds. Interestingly, the VTE is more common during the pregnancy, whereas the pulmonary embolism is more frequent in postpartum period. There are various risk factors for the VTE and pulmonary embolism in these patients. The important risks are improper thromboprophylaxis, obesity, and multigravida. The clinical parameters and the d-dimer are not used for diagnosis of thromboembolism during pregnancy and in the postpartum period. The compression ultrasonography (CUSG) is commonly used for VTE diagnosis; for the pulmonary embolism diagnosis, one has to consider the radiation hazard to the fetus as well as to the mothers. Ventilation/perfusion scan is the imaging of choice for patient who has respiratory signs with normal chest radiograph. If chest X-ray is abnormal with suspicion of peripartum pulmonary embolism (PPE), the choice should be computed tomographic angiography. Heparin and its derivatives remained the anticoagulation of choice for the treatment of VTE as well as the PPE, as it is a shorter acting, easy to reverse with protamine sulfate. Proper thromboprophylaxis is the key for prevention of VTE and peripartum pulmonary embolism.
Part of the book: Embolic Disease
Peripartum Cardiomyopathy: Facts and Figures By Nissar Shaikh, Firdos Ummunnisa, Arshad Chanda, Mohammad A. Imran, Adel Ganaw, Umm-e-Amara, Zia Mahmood, M.A. Rahman, Mohammad Nayeemuddin, Moad Ehfeda, Muhammad Zubair, Ahmed Atef Shible, Ranjan Matthias, Muhammad Shakeel Riaz, Hafiz Hamid Habib, Masood Khattak and A.R. Raju Vegesna
Peripartum cardiomyopathy (PPCM) is a rare clinical entity during pregnancy. PPCM is a diagnosis of exclusion. These patients do not have prior history of heart disease, and there are no other known possible causes of heart failure. It is more common in African countries, may be related to the consumption of kanwa, in the postpartum period. The multiparity, African descent and pregnancy-induced hypertension are a few risk factors for PPCM. The exact etiology of PPCM is not known; possible theories range from myocarditis to the maladaptation to the changes of pregnancy. The clinical manifestation varies from shortness of breath to thromboembolic phenomenon. Echocardiography is essential for diagnosis as well as differential diagnosis of PPCM. These patients preferably are managed in tertiary healthcare facilities. Anticoagulation and antiarrhythmic medications are pillars for the management of PPCM patients. If required, mechanical devices should be used temporarily. PPCM patients may need heart transplant. The beneficial role of bromocriptine and immunosuppression is not clear in PPCM patients. Subsequent pregnancies should be avoided to prevent the PPCM occurrence.
Part of the book: Inflammatory Heart Diseases
Cerebral Arteriovenous Malformation from Classification to the Management By Nissar Shaikh, Aisha Al-Kubaisi, Muhammad Mohsin Khan, Adnan Khan, Zia Mahmood, Arshad Chanda, Adel Ganaw, Gamal Al-Ameri, Mostafa Rezk, Moad Ehfeda, Muhammad Zubair, Jazib Hassan and AR Raju Vegesna
Cerebral arteriovenous malformations (cAVMs) are the rare neurosurgical emergency. cAVM is an abnormal vascular web, composed of nidus, feeding artery and draining veins. It commonly occurs in the supratentorial area of the brain. The common grading system used in cAVM is Spetzler-Martin grading, which takes into consideration the size of nidus, the location of cAVM and the venous drainage. The cAVMs may develop flow and pressure-related aneurysms, which will increase the morbidity and mortality in these patients. cAVMs vary in size and undergo growth, remodeling and rarely regression. Most of the cAVMs are asymptomatic, but the common presentation are headache, seizure, intracerebral hemorrhage or focal neurological deficit. The cerebral angiography remains the gold standard for the diagnosis of cAVM. Management of the cAVM includes medical therapy, surgical excision, radiosurgery and embolization.
Part of the book: Vascular Malformations of the Central Nervous System
Pulmonary Embolism in COVID-19 Patients: Facts and Figures By Nissar Shaikh, Narges Quyyum, Arshad Chanda, Muhammad Zubair, Muhsen Shaheen, Shajahan Idayatulla, Sumayya Aboobacker, Jazib Hassan, Shoaib Nawaz, Ashish Kumar, M.M. Nainthramveetil, Zubair Shahid and Ibrahim Rasheed
COVID-19 infection affects many systems in the body including the coagulation mechanisms. Imbalance between pro-coagulant and anticoagulant activities causes a roughly nine times higher risk for pulmonary embolism (PE) in COVID-19 patients. The reported incidence of PE in COVID-19 patients ranges from 3 to 26%. There is an increased risk of PE in hospitalized patients with lower mobility and patients requiring intensive care therapy. Obesity, atrial fibrillation, raised pro-inflammatory markers, and convalescent plasma therapy increases the risk of PE in COVID-19 patients. Endothelial injury in COVID-19 patients causes loss of vasodilatory, anti-adhesion and fibrinolytic properties. Viral penetration and load leads to the release of cytokines and von Willebrand factor, which induces thrombosis in small and medium vessels. D-dimers elevation gives strong suspicion of PE in COVID-19 patients, and normal D-dimer levels effectively rule it out. Point of care echocardiogram may show right heart dilatation, thrombus in heart or pulmonary arteries. DVT increases the risk of developing PE. The gold standard test for the diagnosis of PE is CTPA (computerized tomographic pulmonary angiography) which also gives alternative diagnosis in the absence of PE. Therapeutic anticoagulation is the corner stone in the management of PE and commonly used anticoagulants are LMWH (low molecular weight heparin) and UFH (unfractionated heparin). Mortality in COVID-19 patients with PE is up to 43% compared to COVID patients without PE being around 3%.
Part of the book: New Knowledge about Pulmonary Thromoboembolism
Preeclampsia: From Etiopathology to Organ Dysfunction By Nissar Shaikh, Seema Nahid, Firdous Ummunnisa, Ifrah Fatima, Mohamad Hilani, Asma Gul, A. Al Basha, W. Yahia, F. Al Hail, H. Elfil, E. Abdalla, M.M. Nainthramveetil, M.A Imraan, Muhammad Zubair, Sibghatulla Khan, N. Korichi, S. Alkhawaga, H. Ismail, S. Yaqoob and Mashael Abdulrahman M.S. Al Khelaifi
Preeclampsia is a hypertensive disorder of pregnancy affecting 6–12% of the population. There are various risk factors for the development of preeclampsia, ranging from advanced maternal age to genetics. The proposed etiologies for preeclampsia are abnormal placentation, immunological intolerance, endothelial damage, and genetic inheritance. The pathogenesis includes endothelial activation and dysfunction leading to vasospasm. Preeclampsia is divided into two stages: asymptomatic and symptomatic stages. Preeclampsia causes multiple organ involvement, namely central nervous system, respiratory, cardiovascular, hematological dysfunction, HELLP (hemolysis elevated liver enzymes, low platelets) syndrome, endocrine, renal, hepatic, and uteroplacental dysfunction. These organ dysfunctions increase morbidity and mortality in preeclamptic pregnant patients.
Part of the book: Preeclampsia
Aneurysmal Subarachnoid Haemorrhage (aSAH) and Hydrocephalus: Fact and Figures By Nissar Shaikh, Arshad Chanda, Kazim Mohammed, Ahmed Balfaqih, Muhammad Mohsin Khan, Seema Nahid, Abdelrahman Balal, Muhammad Zubair, Rahman MA, Hossam Algallie, Gamal Al-Ameri, Abdulnasser Thabet and Ali Ayad
Hydrocephalus (HCP) occurs due to the injurious effect of subarachnoid haemorrhage (SAH). It causes increased morbidity and mortality. It can be acute and frequently occurs within 48 hours and up to 7 days. Subacute hydrocephalus may occur up to 14 days and is chronic if remained or develops after 2 weeks of the subarachnoid haemorrhage. Acute hydrocephalus after aneurysmal subarachnoid (aSAH) bleeding is non-communicating or obstructive and occurs due to physical obstruction by a clot, the effect of blood in the subarachnoid space, and inflammation. Chronic hydrocephalus is due to fibrosis and adhesion, which hampers cerebrospinal fluid (CSF) absorption and increased secretion of CSF from gliosis. Various risk factors for developing hydrocephalus in aneurysmal subarachnoid haemorrhage patients range from female gender to high severity scores. Acute hydrocephalus frequently requires diversion drainage of CSF by external ventricular drain (EVD); it usually subsides within a week, and EVD is removed. Fewer patients will develop or continue to have hydrocephalus, requiring either short or longer shunting of the CSF namely by ventriculoperitoneal shunt or other modes of CSF drainage.
Part of the book: Frontiers in Hydrocephalus
Acute Management of Heat Stroke: Facts and Figures By Gamal Al-Ameri, Waleed Salem, Galal Alessai, Mohammed Hellboob, Mubarak Alhatemi, Umme Nashrah and Nissar Shaikh
Heat-related illnesses range from heat exhaustion to heat stroke. Heat stroke is a life-threatening medical emergency causing multiple organ dysfunction that if not treated, can be fatal. It is a severe heat illness with a body temperature of more than 400c and organ dysfunction. Epidemiology of heat stroke varies depending on geographic location, and reported incidences range from 1.98 to 2.89/100000 per year. Heat stroke is classified as exertional or non-exertional. Pathophysiology is exposure to higher temperatures with impaired thermoregulation. Patients will present with high core body temperature; tachypnea, tachycardia, and hypotension may be present. The manifestations of organ dysfunction range from coagulopathy to altered levels of consciousness, and pulmonary edema. Accurate core body temperature measurement with clinical manifestations will diagnose the heat stroke. Early diagnosis, earlier temperature management, and organ supportive care are essential.
Part of the book: Heat Illness and Critical Care
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