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Acute Respiratory Distress Syndrome

  • The novel coronavirus was named as the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) due to its high similarity to SARS-CoV, which caused acute respiratory distress syndrome (ARDS) in 2002–2003.
  • SARS-CoV-2 virus primarily affects the respiratory system causing wide variety of respiratory symptoms which can range from symptoms of lower respiratory tract infection to severe hypoxia to acute respiratory distress syndrome within a very short span of time.

Epidemiology

  • Incidence is higher in the elderly and much lower in children
  • Higher mortality rate is seen in the elderly.

Pathophysiology

  • ARDS arises as a complication of COVID-19 infection due to acute inflammation of the alveolar space which prevents normal gas exchange. The increase in proinflammatory cytokines within the lung leads to recruitment of leukocytes, further propagating the local inflammatory response
  • The cytokine storm and the deadly uncontrolled systemic inflammatory response resulting from the release of large amounts of proinflammatory cytokines including interferons and interleukins and, chemokines by immune effector cells resulting in acute inflammation within the alveolar space. The exudate containing plasma proteins, including albumin, fibrinogen, proinflammatory cytokines and coagulation factors will increase alveolar-capillary permeability and decrease the normal gas exchange and plasma proteins, including albumin, fibrinogen, proinflammatory cytokines and coagulation factors.
  • The COVID-19 patients with ARDS show elevated levels of IL-6, IFN-a, and CCL5, CXCL8, CXCL-10 in serum compared to those with the mild-moderate disease [11]
  • This inflammatory process leads to the fibrin deposition in the air spaces and lung parenchyma and contributes to hyaline-membrane formation and subsequent alveolar fibrosis.
  • Patients infected with COVID‐19 exhibit coagulation abnormalities.[1] This procoagulant pattern can lead to acute respiratory distress syndrome.

Diagnosis

Laboratory findings

  • Blood plasma has elevated levels of IL-6, IL-1, tumor necrosis factor-α (TNF α) and C-reactive protein.
  • Mild thrombocytopenia
  • Increased D-dimer levels. The elevated level of D-dimer is strongly associated with a higher mortality rate.
  • Increased fibrin degradation products
  • Increased fibrinogen.
  • Prothrombin time and activated partial thromboplastin time may be slightly elevated.

Imaging studies

  • Chest CT scan shows characteristic ground-glass opacities (GCO). This indicates the presence of exudate in the bronchoalveolar airspace.
  • Lung biopsy shows fibrin deposition.

Signs and Symptoms

Treatment

Fluid and electrolytes management

Glucocorticoids

Mechanical Ventilation

  • Majority of COVID-19 patients with ARDS require mechanical ventilation for two weeks or more. The aim is to maintain oxygen saturation between 90 and 96%. The severe hypoxemia of the COVID-19 ARDS best responds when Positive end-expiratory pressure (PEEP) is high with Pplat ≤30 cm H2O. It is beneficial if the physician starts with higher than usual levels o PEEP (10 to 15 cm H2O).

Anticoagulant or thrombolytic therapy

  • Fibrinolytic drugs such as tissue-type plasminogen activator (tPA) degrade pre-existing fibrin in the lungs.
  • Nebulizer plasminogen activators may provide more targeted therapy to degrade fibrin and improving oxygenation in critically ill patients. It is in Phase II of the clinical trial.

Prevention

  • The ARDS patients have an increased risk of hospital-associated venous thromboembolism (VTE). Due to this reason, it is advised to take low molecular weight heparin (LMWH) prophylactically in patients who do not have the contraindications. Studies have shown that the heparin, either unfractionated or LMWH, can also reduce inflammatory biomarkers hence could help in reducing the inflammation.

Cardiovascular Disorders and COVID-19

Spontaneous coronary dissection

Pathophysiology In patients with an inflammatory overload, a localized inflammation of the coronary adventitia and periadventitial fat can occur. This could lead to the development of sudden coronary artery dissection in a susceptible patient. Signs and symptoms Treatment




 
 
 
 
 
 
 
Neurofibromatosis
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Neurofibromatosis 1
 
 
 
 
 
Neurofibromatosis 2
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
NF1 tumor suppresor gene Mutation located on chromosome 17, encodes for neurofibromin
 
 
 
 
 
NF2 tumor suppresor gene Mutation located on chromosome 22, encodes for merlin
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
clinical features: Cafe-au-lait spots, multiple neurofibromas and lisch nodules
 
 
 
 
 
Clinical features: bilateral acoustic neuromas
 
 
 

Features of Wenicke-Korsakoff Syndrome
Associated conditions
  • Chronic alcoholism (most common).
  • Malnutrition.
Pathophysiology Thiamine deficiency impairs ATP generation leading to neuronal dysfunction and death. It mostly has paraventricular lesions involving mammillary bodies and dorsomedial bodies.
Clinical findings
  • Confusion.
  • Oculomotor dysfunction (horizontal nystagmus and bilateral abducens palsy)
  • Postural and gait ataxia.
  • Memory impairment (permanent).
Treatment
  • Intravenous thiamine.
  • Administration of glucose before the thiamine can worsen the symptoms.
Acne vulgaris
Clinical features
  • Comedonal acne:Closed or open comedones on forehead, nose and chin.
  • Inflammatory acne: Small, erythematous papules and pustules.
  • Nodular acne: Large painful nodules; sinus tracts and scarring.
Pathogenesis
  • Hyperkeratinization and obstruction of the pilosebacous follicles.
  • Sebaceous gland enlargement and increased sebum production.
  • Metabolism of sebaceous lipids by Cutibacterium acnes and release of inflammatory fatty acid.
  • Follicular inflammation and rupture,
Risk factors i) Increased circulating androgen (e.g. PCOS, puberty)

ii) Mechanical trauma/friction (excessive scrubbing, tight clothing)

iii) Comedogenic oil based skin and hair products.

iv) Excessive heat.

v) Obesity


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Criteria for the diagnosis of SLE
Clinical features Characteristics
1)Malar rash Fixed erythema, flat or raised, sparing the nasolabial folds
2)Discoid rash Erythematous raised patches with adherent keratotic scarring and follicular plugging.
3)Photosensitivity Rash due to unusual reaction to sunlight.
4)Oral ulcer Oral or nasopharyngeal ulcers, which may be painless.
5)Arthritis Non-erosive arthritis, involving >2 peripheral joints.
6)Serositis Pleuritis or pericarditis
7)Renal disorder Persistent proteinura ( >0.5g/24hrs) or cellular casts (red cell, granular or tubular).
8)Neurological disorder Seizure or psychosis, in the absence of provoking drugs or metabolic derangement.
9)Hematological disorder Haemolytic anemia or leucopenia (<4 x109) or lymphopenia (<1x109) or thrombocytopenia (<100x109) in the absence of offending drugs.
10)Immunological Abnormal titre of Anti-DNA antibodies or presence of Sm antigen or positive antiphospholipid antibodies.
11)Anti-nuclear Antibody (ANA) Abnormal ANA titre measured by immunofluorescence
Diagnosis of SLE is made in an adult if 4 out of 11 features are present either serially or simultaneously.
  • Erythematous raised patches with adherent keratotic scarring and follicular plugging.
 
 
 
 
 
 
 
Congenital anomalies of the urinary system
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Kidneys
 
Renal pelvis
 
Ureter
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Renal agenesis
 
Duplication of renal pelvis
 
Duplication of ureter
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Renal ectopia
 
 
 
 
 
Congenital megaureter
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Horseshoe kidney
 
 
 
 
 
Post-caval ureter
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Unilateral fusion
 
 
 
 
 
Ureterocele
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Congenital cystic kidney
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Infantile polycystic kidney
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Unlilateral Multicystic Kidney
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Simple cyst of the kidney
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Aberrant renal vessels
 
 
 
 
 
 
 
 
 







T
 
 
 
 
 
 
 
 
 
Mycosis fungoides
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Stage IA-IIA
 
Stage IIA
 
 
Stage III
 
 
Stage IV
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

• Expectane policy
• Topical steroides [IV-A]
• nb-UVB[III,A]
• PUVA [III-A]
• Topical mechlorethamine [II,B]
• Local RT [IV,A]
 

• Skin direct therapy(SDT) + local radiotherapy
• ST[III+A]
• (SDT+) retiods[III,B]
• (SDT+) IFN a {III,B]
• TSEBT [III,A]
 
 

• (SDT+) retinoides
• (SDT+) IFNa
• ECPI INFa +/- rtinoides
• Low dose MTX
• [IV-B]
 
 

• Gemcitabine
• Liposomal doxorubicin
• Brentuximab vedotin[II,B]
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

• (SDT+) retinoides [III,B]
• (SDT+) IFNa [III,B]
• Retinoides +IFN a [II,B]
• TSEBT [IV,A]
 

• Gemcitabin [IV,B]
• Liposomal doxorubicin [IV,B]
• Brentuximabvedotin [II,B]
• Combinatio Cht [Iv,B]
• AlloSCT[V,C]
 
 
TSEBT[LV,B]
 
 

• Combination Cht [IV,B]
• AlloSCT [V,C]
 
 
 
 
  1. Ranucci M, Ballotta A, Di Dedda U, Bayshnikova E, Dei Poli M, Resta M; et al. (2020). "The procoagulant pattern of patients with COVID-19 acute respiratory distress syndrome". J Thromb Haemost. doi:10.1111/jth.14854. PMID 32302448 PMID: 32302448 Check |pmid= value (help).
  2. Yang X, Yu Y, Xu J, Shu H, Xia J, Liu H; et al. (2020). "Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study". Lancet Respir Med. 8 (5): 475–481. doi:10.1016/S2213-2600(20)30079-5. PMC 7102538 Check |pmc= value (help). PMID 32105632 PMID: 32105632 Check |pmid= value (help).
  3. Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J; et al. (2020). "Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China". JAMA. doi:10.1001/jama.2020.1585. PMC 7042881 Check |pmc= value (help). PMID 32031570 PMID 32031570 Check |pmid= value (help).