Case Study: A COVID Patient and Ineffective Therapy


Care Report: 44 year old female with a history of insulin requiring diabetes mellitus presents with increasing cough, shortness of breath and fever.


History of Present Illness:

She reported to the emergency department five days prior to admission with the following symptoms:

  • increased body aches
  • nausea, vomiting and poor appetite for the last few days
  • chest pain with inspiration
  • shortness of breath
  • cough possibly going back 5 weeks, per patient


Past Medical History:

  1.  Hypertension
  2.  Obesity BMI 33
  3.  Insulin-dependent diabetes with diabetic neuropathy
  4.  Hyperlipidemia

Meds:  Insulin, Gabapentin, atorvastatin occ.


Social History: no smoking or alcohol


Physical Examination.  The vital signs and exam (normal if not listed):

T 99 F, BP 144/78, RR 15, Pulse OX 95% Room air, BMI 34

  • Gen: no distress, non-toxic
  • Chest:  Lungs clear, non-labored
  • Neurologic: Mental status intact

The bloodwork at the Emergency department:

  • WBC 6.9
  • Glucose 411
  • BUN 28
  • Creatinine 1.6
  • Alb 2.9
  • LFTs normal

In the ER she was found to have some changes on a radiograph:


Initial CXR “atypical pneumonia multilobar”


Since she was not with any respiratory distress and did not have a low oxygen level, she was discharged and asked to follow-up closely.   In the ER, she received IV antibiotics ceftriaxone and azithromycin and sent out to pick up amoxicillin/clavulonic acid.

She returned 2 days after, with worsening shortness of breath and persistent dry cough.  She has had increased weakness and has chest pain with inspiration.

In the triage, she was found to have a pulse ox of 86% on room air.

Exam:  T: 99.6, BP 147/47, pulse ox 95% on 5 L nasal cannula.

  • Gen: She looks exhausted and in mild respiratory distress
  • Pulm:  Poor air movement bilaterally; scattered rhonchi, no wheezing.

The Repeat ER labs:

  • Glucose 609
  • WBC 5.6
  • Sodium 129
  • Creatinine 1.7 (baseline was 0.7 to 1.0)
  • Procalcitonin 0.27
  • Lactate Normal

Follow-up CXR: 


CXR:  Worsening changes



  • The patient was found to have COVID-19 PCR positive.  
  • She developed worsening shortness of breath and was placed on a non-rebreather and transferred to the ICU for increasing oxygen requirements.
  • She was intubated on account of worsening status
  • She was initiated on hydroxychloroquine protocol on account of respiratory status
  • Her Max creatinine was 4 and she was initiated on dialysis.
  • A trial of toclizumab was begun.



Follow-up Radiograph 7 days from initial.



Impression:  COVID-19 with severe pneumonitis and respiratory failure along with Acute Kidney Injury.



The patient presented with dry cough, fever, chest pain with inspiration and worsening shortness of breath.  She interestingly had presented several weeks before with a cough, though was not found to have any concerning features.  It is conceivable that the process began more recently and was interpreted by the patient as the same cough.

The typical signs and symptoms of mild COVID-19 disease include a cough, fever and sore throat.  However, a small percent, approximately 5-10%, may progress to a more severe presentation.  Risk factors are usually present, the most is age > 75 years, followed by 65-74, followed by hypertension, diabetes mellitus and obesity.  This patient had multiple metabolic consequences of her obesity.

She progressed to a more severe cough and shortness of breath.  The average time of developing worsening shortness of breath is approximately 8 days after the onset of symptoms.  Intervention requiring intubation (placing a endotracheal tube to ventilate) usually occurs 3-4 days later in approximately 60-80% of patients with Severe COVID-19.  From the Wuhan patient data, once ventilated mortality rates can be in the 50-60% range.


The pathology of diseased tissue can provide a lot of detail in what occurs when a patient has severe COVID-19.  Biopsies taken from patients who had COVID-19 show desquamation (loss of lining) of pneumocytes and hyaline membrane foundations – both features of acute respiratory distress syndrome (ARDS).  There were lymphocytic infiltrates and pulmonary edema (fluid swelling).   The cells were multinucleated, a finding seen in viral infected cells.  Viral cytopathic-like changes were seen.  Other biopsies have shown thrombosis (clots), hemorrhage (bleeding), and necrosis (tissue death), as well as bronchoalveolar fibrin plugs.

Clinical Finding of Hypoxia

Does COVID-19 attack the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism?  Does not fit the likely physiologic model.

Although we are still developing a clear understanding of the pathophysiology of covid-19 and severe disease, it likely does not include the article regarding heme scavenging. This was a model and not confirmed in actual studies. Additionally this was a thought experiment from the reports of possible benefit from chloroquine and was inherently biased.  The researchers may have asked, ”why would chloroquine be beneficial?” From reading the profiles of the researchers, this non-peer reviewed study was written by non-cliniciansthat may not be informed of some of the intricacies of gas exchange. Now studies have really even questioned the benefit of hydroxychloroquine or chloroquine with no improvement seen in small controlled studies.

You can look at this as the question of shunting – where blood is escaping oxygenation, perfusion, where blood is not getting oxygenated in the same concentration as it gets delivered to the alveolar membrane or diffusion, where the oxygen is not able to diffuse across the membrane and into the alveolar capillaries.  If iron were removed from red cells, to flow freely, it might cause something similar to iron deficiency — but it wouldn’t cause HYPOXIA.  It would make the heart increase its rate to improve perfusion.

What is happening in the tissues is necrosis (tissue death, hemorrhage and thrombosis). There are fibrin-rich bronchoalveolar plugs. The necrosis and hemorrhage is leading to the CT findings.  These conditions impair diffusion of oxygen into the alveolar capillaries. The pathology alone is enough to explain how this process may be occurring. There are essentially barriers for oxygen delivery from those changes and thrombosis in pulmonary vessels which impair oxygenation.

People with severe covid-19 often present with low oxygen saturations when they come in – there is lung disease but not as much edema as typical ARDS.  Nevertheless, and the pathology supports this, it approaches what is occurring with ARDS. Some describe the process as “dry,” or having two forms of respiratory failure, dry or wet.

They often still have some pliability of their airways. However, ventilation could induce lung injury from high pressures – including the higher positive end-exploratory pressures (PEEP) used for typical ARDS.  It is therefore recommended to provide supplemental oxygen under high flow and other noninvasive ventilatory methods rather than intubation.

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