Some of the many but not all causes include:
♦️Thrombi, Clots & Hypercoaguable States
♦️Vessel Stenosis & PVD (often from Atherosclerosis)
♦️Disorders affecting viscosity (PCV, Waldenstrom, etc)
♦️Sickle Cell
The medical community is divided when it comes to treating #COVID19. Various debates/theories dominate #MedTwitter & #FOAMed. Im glad to see these discussions & our progress, however patients sometimes get caught in the middle….
This thread’s intention is to simply share observations & the experience of a #COVID19 patient code named “Halo” (yes consent received by mother) whose story might seem unique but sadly a common occurrence throughout many NYC hospitals
Halo, A mid 30 year old w/#COVID19 symptoms (Febrile/SOB) for a week presented to the ED & had this CXR👇
As ED physicians, the difficult decision of disposition has never haunted us more these days when they’re like Halo: alert, talking & do not appear clinically ill
As a result, theres a very large number of “Happy Hypoxic” patients who have been tolerating HFNC for hours & sometimes for days. SpO2 continues to remain unreliable (as do certain "traditional" exam findings of respiratory distress). PaO2s continue to correlate
The oxygen requirement these patients need is very high. Hospitals w/lower volumes of #COVID19 patients should start from now in securing the appropriate resources and have contingency plans to accommodate for this
As physicians we see a low SpO2 combined with a low PaO2 & the knee jerk reaction is early intubation instead of assessing patient's overall clinical picture including their work of breathing & mental status. Here's a walk through what happens after...
Following intubation, patients are put on higher PEEPs which combined w/ACE-receptor effects of virus worsens their already slightly elevated creatinine. Higher PEEPs causing increased thoracic pressure understandably leads to hypotension so patients are then given fluids