COVID-19: From authors' diary for health care workers

I want to write this post and acknowledge that the pandemic is a very stressful time for healthcare workers. 

We are looking at the epidemiology that shows the increase in mortality related to the COVID-19 disease. Even though we see death everyday, addition of deaths due to SARS-CoV-2 is heartbreaking. Thoughts about not having enough ventilators, not having proven medical therapies, or a vaccine in the near future are distressing. It is in our inherent nature as healthcare professionals to try and help, it's saddening when we can't. 

Hearing the news is also very depressing. Some don't believe it. Some aren't serious enough... Yet. But when you hear the stories instead of looking at the numbers, it becomes real. How strange must it be, to be in quarantine and see your old grandparent go to the hospital alone? How sad must it be to think that it may be the last time that you see them? 

There are concerns about our safety as healthcare workers. We are being exposed on a daily basis and there are concerns about having not enough personal protective equipment such as masks in the future. Even worse, there are concerns about our families safety. We expose them every time we come home. 

I just want to tell you that all your anxieties and concerns are valid. You're not the only one thinking about these things. As we fight this pandemic together, our mental health is important. I'm proud of you for being concerned. I'm proud of you for continuing to fight everyday. 

If you are a health care provider and are distressed by this like I was and want to talk about it, email me at medicowesome@gmail.com. We also have a well being group on Whatsapp to help each other stay strong! 

I was recently talking to a colleague about how we have chosen this profession because this is what we always wanted to do - treat patients. We spoke about the retired physician in Italy who came back to work for his patients. It's noble. It's humbling. If we don't take care of the sick, who will?

-IkaN

COVID-19: Water transmission and the effects of heat on the SARS-CoV-2 virus

Hi!

I am going to be writing a series of COVID-19 posts and answering frequently asked questions by patients. Today's post is about water transmission and the effects of heat on the SARS-CoV-2 virus.

Mnemonic for Foley’s Catheter: French scale & Color code

Video by Drashtant

Recent updates about treatment of COVID19

All things you need to know about COVID19 

https://www.youtube.com/watch?v=A6WpCkjqJSM

Recent Updates: 

At present Best Option = HydroxyCQ +/- Azithromycin 

HydroxyCQ for 10 day ( 200 mg TDS ) 

As ACE 2 enzyme is receptor for SARS-Cov-2 & these RAS inhibitors ⬆️ ACE2 enzyme. So hypothetically, there's an ⬆️ Risk of Covid19. But the guidelines recommend that ACEI / ARBs should not be discontinued. 

Drugs under Clinical Trials:

Remdesivir (USA) 

Ritonavir-Lopinavir 

Tocilizumab (IL6) 

Sarilumab (IL6) 

Favipiravir+ Tocilizumab 

Meplazumab (CD147) 

Fingolimod 

Darunavir + Cobicistat 

Which Rx is used in your country now?  Please comment below ⬇️

Thank you.. 

- Drashtant 

Isatuximab (Novel monoclonal antibody)

Isatuximab (a novel monoclonal antibody that binds
selectively to CD38), which is widely expressed on the plasma
cells, and kills myeloma cells via multimodal mechanisms
including antibody-dependent cellular cytotoxicity,
antibody-dependent cellular phagocytosis, complement-
dependent cellular cytotoxicity, and immune cell
depletion or inhibition of immunosuppressive cells, as has been described with daratumumab.

 Additionally, isatuximab, similar to other CD38 antibodies, modulates
the NADase enzymatic activity of CD38.
However, isatuximab differentiates itself from daratumumab in its
ability to induce direct apoptosis without cross-linking, and in its binding epitope.

Isatuximab is approved in combination with pomalidomide and dexamethasone for adult patients with multiple myeloma who have received at least two prior therapies including lenalidomide and a proteasome inhibitor.

A pretty amazing mechanism, right?


Kirtan

How to approach Ankle sprain

Hi!

I sprained my ankle and thought of making a video on it 

-Drashtant

Layers Of The Abdomen

SUB - Skin

CUTANEOUS- Camper's Fascia

SYSTEM - Scarpa's Fascia

EXITS - External Oblique

INTESTINAL- Internal Oblique

TRANSPORTw/ - Trs Abdominis 

FREE- Fascia Transversalis 

EXIT- Extra Peritoneal C/T 

PASS- Parietal peritoneum 

Everything you need to know about coronavirus COVID-19

Resources: CDC, UpToDate, WHO website.
Video by Drashtant Prajapati, MBBS.

Pulsus paradoxus concept

-IkaN

Everything you need to know about coronavirus COVID-19

Resources: CDC, UpToDate, WHO website.
Video by Drashtant Prajapati, MBBS.

Tricuspid Annular Plane Systolic Excursion (TAPSE) concept

Acquired coagulopathy

Apart from congenital disorders, various clinical scenarios can give rise to altered hemostatic patterns leading to the state of so-called "acquired coagulopathy".

1.) Due to Factor inhibitors:
Classically it is seen in pregnant patients and those with lymphoproliferative disorders like CLL. However, it could be idiopathic.
Usually, it leads to the acquired factor Vlll and V deficiency.

Mixing studies are employed to differentiate between acquired and congenital factor deficiency. Failure of correction of clotting assays after mixing studies suggests the presence of inhibitors.

2.) Amyloidosis
Sequestration of Factor X by amyloid fibrils leads to an acquired deficiency-like state. Amyloid vasculopathy along with factor X deficiency often leads to purpura and ecchymosis in these patients.

3.) Myeloproliferative neoplasms
Apart from acquired vWD due to loss of HMW vWF multimers, acquired factor V deficiency can also be seen. This has been attributed to adherence of Factor V to megakaryoblasts similar to the relation between factor X and amyloid fibrils. However, severe clinical manifestations might not necessarily reflect upon clotting assays or factor levels with the latter suggesting functional factor V deficiency.

3.) Thrombotic microangiopathies and DIC
Usually leads to both thrombotic and bleeding manifestations. The spectrum of TMA includes HUS, aHUS, TTP, HELLP syndrome, DIC, cAPLA, scleroderma renal crisis, malignant hypertension, and radiation or HSCT-induced vasculopathy.

4.) Coagulopathy of liver failure
Classically seen in the setting of fulminant liver injury which may be due to the infections, drugs, autoimmune hepatitis, ischemic hepatitis/shock liver, or rarely in Wilson's disease due to massive hepatocyte destruction.
One of the hallmark lab findings includes normal factor VIII levels. This is due to the fact that factor VIII, unlike other factors, is chiefly produced by endothelial cells rather than by hepatocytes. In fact, due to its reduced metabolism by hepatocytes in the state of liver failure, factor VIIl levels are often elevated.

Other miscellaneous causes include Acute fatty liver of pregnancy, fat embolism syndrome, amniotic fluid embolism, and other pregnancy-associated complications.

- Kirtan Patolia

Acquired Von willebrand disease

Von Willebrand disease is one of the most commonly encountered congenital bleeding disorders in clinical practice. Broadly speaking they are classified as type 1, 2A, 2B, 2M, 2N, and 3. Each one of them is distinct from the other in subtle ways.

However, it could be acquired in a number of ways.

 a.) In patients with thrombocytosis > 1 million cells/ microliter, especially in essential thrombocythemia, loss of HMW  vWD multimers leads to reduced vWF Ristocetin activity: vWF antigen ratio (<0.6)  suggesting type 2 like pattern.

 b.) In patients with aortic stenosis, due to extreme shear stress, vWF unfolds prematurely at the site of the valve revealing ADAMTS13 binding sites, ultimately resulting in its cleavage and loss of HMW multimers. So basically, it could be visualized as the pattern that is just opposite to TTP wherein defective ADAMTS13 activity results in excess of HMW vWF multimers.

It is often associated with either angiodysplasia or AVMs of the GI tract that further predisposes to bleeding. Although the exact pathogenesis of these lesions is not understood, one postulated mechanism suggests chronic colonic ischemia leading to sympathetic nervous system-induced vasodilation as a potential culprit.
 In this context, it is also known as Heyde's syndrome.

c.) Sometimes in severe hypothyroidism, often the production of vWF by endothelial cells itself is markedly reduced.

d.) Rarely in the setting of multiple myeloma and various other neoplasms, tumor cells express the excess of Gpllb/llla leading to enhanced clearance of vWF from circulation.

One of the common lab findings in acquired vWD is reduced vWF Ristocetin activity: vWF antigen ratio pointing to the disproportionate decrease in activity compared to antigen levels.
It is due to the loss of HMW  multimers.

- Kirtan Patolia