2/ NS can cause coagulopathy
- NS dilutes clotting factors ➡️ impairing coagulation and hemostasis.
-NS can cause a functional impairment of thrombin and fibrinogen
- ⬆️ disruption of existing clots.
- acidic milieu can also ⬇️ clot formation/stability
4/ Increasing edema:
-NS can increase vascular permeability driving leak of proteins into the interstitial compartment
-can drive the dilatation of vessels➡️ increase cardiovascular stress
-NS can also ⬆️ interstitial edema
- only 20% of infused NS remains intravascular
5/ ⬆️disruption to the vascular endothelial layer by NS induced acidosis:
This is a mechanism explained in animal models where the endothelial glycocalyx is disrupted resulting in more edema.
6/ Fig C- Crystalloids damage EGL layer and worsen edema
7/ NS induced acidosis can impair cardiac contractilty and also decrease BP.
That may account for a precipitous drop in BP soon after a temporary recovery of BP with a bolus.
This can also be attributed to distribution of fluids across compartments including the interstitium.
8/ Saline causes hemodynamic instability:
- ⬆️vasocdilation and in this small study there was a finding that patients receiving NS required vasopressors more frequently.
9/ ⬆️ Inflammation with NS
- LR favored in acute pancreatitis - NS can worsen inflammation and necrosis in this condition.
Pts with acute panc. had a no significant trend towards higher SIRS
- higher levels of CRP/ other pro-inflammatory cytokines with NS
10/ Inflammation ⬇️ LR
In vitro, LR inhibited the induction of inflammatory phenotype of macrophages and NF-κB activation. This effect was not observed when using Ringer's solution without lactate, suggesting a direct anti-inflammatory effect of lactate
1/8 You start SQ insulin on a patient and they develop peripheral edema ?
What is the mechanism of "Insulin edema" ? #MedTwitter#MedStudentTwitter
2/8 This condition was initially reported by Aaron Leifer, M.D. in 1928 in a 41-year-old male patient started on an insulin regimen which was published in JAMA.
Leifer A. A CASE OF INSULIN EDEMA. JAMA. 1928;90(8):610–611. doi:10.1001/jama.1928.92690350001012
3/8 The severity of edema is usually mild, involving the limbs, sparing the torso and face.
Resolution is usually seen after one to two weeks of conservative treatment with fluid and salt restriction and may or may not involve the use of diuretics grepmed.com/images/6334/dr…
1/ 10 The most recognized form of Non-Cardiogenic pulmonary edema(NCPE) is ARDS, however the scope of NCPE is much broader with many causes. One particular cause of NCPE we encountered was due to opoid use which is explored in this #medtweetorial #MedTwitter#MedStudentTwitter
2/10 The onset of noncardiogenic pulmonary edema after opioid overdose was first described by Osler
during an autopsy in 1880
Osler W. Oedema of the left lung — morphia poisoning: Montreal General Hospital Reports Clinical and Pathological. Montreal: Dawson Bros., 1880:291.
3/10 Its presentation and clinical course was not appreciated until the 1950s-60s.
-mechanism is known to involve ⬆️ alveolar capillary permeability
-Opioid-related NCPE presents as :
dyspnea +/- pink, frothy pulmonary secretions
+ hypoxia
Other criteria is detailed below:
1/ Is bandemia with a normal WBC count concerning for a lethal infection?
It's a very interesting concept which I've faced and will explore below : #MedTwitter#MedStudentTwitter#FOAMed
2/“Left shift” means that a particular population of cells is “shifted” towards more immature precursors
Josef Arneth (1873-1955) described this left-shift term.
3/Mechanical hematologic counters were used early on last century which perpetuated the term" left shift" with the manual counting of immature neutrophils which were towards the left side of the mature cells on the counter.
1/ "Don't forget to correct that phosphate so that the it can help the patient recover from acute respiratory failure !" This concept triggered a lot of questions on rounds.
It's worth taking a quick look at this association ! #medtwitter#MedStudentTwitter#FOAMed#phosphate
2/⬇️Phosphate leads to ⬇️red cell 2,3-DPG and a reduction in ATP.
⬇️Phosphate diverts glucose -> 1,3-DPG into the Rapoport-Leubering pathway away from ATP generation towards producing 2,3-DPG so that the oxygen affinity of RBC's does not increase and the tissues receive O2.
3/⬇️Phosphate does also impact RBC survivability with a
⬆️hemolysis, ⬇️in RBC deformability, ⬇️ capillary transit and ⬇️GSH.
2/Interestingly , anemia of hospitalization is commonly thought to be due to
- phlebotomy
- IVF
- invasive procedures/ bleeding etc
However, prolonged bed rest can contribute to a drop in your pts blood count !
Another reason to get our patient's out of bed if possible !
3/Until the mid-20th century, bedrest was considered a benefit that helped people heal. Hippocrates had already noted the risk of loss of muscle, bone and tooth(Chadwick and Mann, 1950)
Today, there is recognition of bedrest’s negative effects on body and the blood volume.