D-dimer
Plasma D-dimer is a product of clot breakdown, released upon degradation of polymerized, crosslinked fibrin. Elevated plasma D-dimer levels indicate that coagulation has been activated, fibrin clot has formed, & clot degradation by plasmin has occurred.
D-dimer has been shown to increase with age, which can cause a ↓ specificity (i.e. more false positive tests) in older patients. Specificity can range from 49-67% in 50 yrs of age, but in older patients (i.e. 80 yrs of age) the specificity is 0-18%
How do you perform age adjusted d-dimer testing?
- Age (yrs) x 10 u g/ L for > 50 yrs of age
- Example: Patient age 88 = age adjusted d-dimer of 880 u g/ L
Satyendra Dhar, MD @DharSaty
#Ddimer #dimer #pathophysiology #hematology #differential #diagnosis #age #adjusted
Lactic acid was first found & described in sour milk by Karl Wilhelm Scheele in 1780. German physician–chemist Johann Joseph Scherer (1841–1869) demonstrated the occurrence of lactic acid in human blood under pathological conditions in 1843 & 1851.
Lactic acid is essentially a carbohydrate within cellular metabolism and its levels rise with increased metabolism during exercise and with catecholamine stimulation. Glucose-6-phosphate is converted anaerobically to pyruvate via the Embden-Meyerhof pathway. Pyruvate is in equilibrium with lactate with a ratio of about 25 lactate to 1 pyruvate molecules. Thus, lactate is the normal endpoint of the anaerobic breakdown of glucose in the tissues.
Satyendra Dhar MD, @DharSaty
#Lacticacid, #Lactate, #Shock,
Mean arterial pressure (MAP)
A common method used to estimate the MAP is the following formula:
* MAP = DP + 1/3(SP – DP) or
* MAP = DP + 1/3(PP)
Where DP is the diastolic blood pressure, SP is the systolic blood pressure, and PP is the pulse pressure.
To perfuse vital organs requires the maintenance of a minimum MAP of 60 mmHg. If MAP drops below this point for an extended period, end-organ manifestations such as ischemia and infarction can occur. If the MAP drops significantly, blood will not be able to perfuse cerebral tissues, there will be a loss of consciousness, and neuronal death will quickly ensue.
Satyendra Dhar MD, @DharSaty
#MAP #meanarterialpressure #pulsepressure #sbp #dbp #perfusion #ischemia
INSULIN CONVERSION
Total daily dose of insulin (TDD) =
N X Wt in Kg
(N= 0.5-1.0 for obese, resistant & most type 2 DM)
Administer:
½ as Basal (Long acting) & ½ in 3 divided doses a day before each meal
Target pre-meal BG < 140 & random BG < 180 in non-ICU pts
For patients who aren’t transitioning from IV insulin or who aren’t on an insulin regimen at home, many experts offer these rules of thumb for estimating total daily dose:
* 0.3 units/kg/day for patients who are lean, on hemodialysis, frail and elderly, insulin-sensitive, or at risk for hypoglycemia;
* 0.4 units/kg/day for a patient at normal weight;
* 0.5 units/kg/day for overweight patients; and
* 0.6 units/kg/day or more for patients who are obese, on high-dose steroids or insulin-resistant.
Satyendra Dhar MD, @DharSaty
#insulin #diabetes #hyperglycemia #dm2 #basalinsulin
C-REACTIVE PROTEIN
Discovered by Tillett & Francis in 1930. First identified as a substance in the serum with acute inflammation that reacted with the "c" carbohydrate Ab of the capsule of pneumococcus.
CRP is a pentameric protein synthesized by the liver, whose level rises in response to inflammation. CRP is an acute-phase reactant protein that is primarily induced by the IL-6 action on the gene responsible for the transcription of CRP during the acute phase of an inflammatory/infectious process.
Lab values vary, and there is no standard at present. However, in general, the result is reported in either mg/dL or mg/L. Hs-CRP is usually reported in mg/L.
Interpretation of CRP levels:
Less than 0.3 mg/L: Normal (level seen in most healthy adults).
0.3 to 1.0 mg/L: Normal or minor elevation (can be seen in obesity, pregnancy, depression, diabetes, common cold, gingivitis, periodontitis, sedentary lifestyle, cigarette smoking, and genetic polymorphisms).
1.0 to 10.0 mg/L: Moderate elevation (Systemic inflammation such as RA, SLE, or other autoimmune diseases, malignancies, myocardial infarction, pancreatitis, bronchitis).
More than 10.0 mg/L: Marked elevation (Acute bacterial infections, viral infections, systemic vasculitis, major trauma).
More than 50.0 mg/L: Severe elevation (Acute bacterial infections).
Certain medications, such as NSAIDs will falsely decrease CRP levels. Statins, as well, have been known to reduce CRP levels falsely. Recent injury or illness can falsely elevate levels, particularly when using this test for cardiac risk stratification. Magnesium supplementation also can decrease CRP levels.
As mentioned above, mild elevations in CRP can be seen without any systemic or inflammatory disease. Females and elderly patients have higher levels of CRP. Obesity, insomnia, depression, smoking, and diabetes can all contribute to mild elevations in CRP, and the results shall be interpreted with caution in individuals with these comorbidities.
Satyendra Dhar MD, @DharSaty
#CRP #C-REACTIVEPROTEIN #inflammation #Hs-CRP
Electrolyte Repletion
Significant electrolyte depletion can result in serious complications. These guidelines are meant to assist with empiric dosing of electrolytes for inpatients. Doses may need to be adjusted based on patient-specific factors, including creatine & cardiac status; & responses to initial doses.
Goal serum potassium concentration 4.0 – 5.0 mEq/L
Goal serum ionized calcium concentration 1.12 – 1.3 mmol/L
Goal serum magnesium concentration 2.0 – 2.4 mg/dL
Goal serum phosphorus concentration 2.7 – 4.6 mg/dL
IV electrolyte replacement can produce life-threatening complications, serious arrhythmias & phlebitis; therefore, supplementation must be carefully monitored. There are multiple underlying factors for electrolyte disorders in adult inpatients, including alterations in absorption, distribution, hormonal, and/or homeostatic mechanisms can all cause disturbances. Treating the underlying cause and prescribing adequate therapy is essential for repletion. In addition, the intracellular vs. extracellular electrolyte concentrations must be considered. Due to distribution variances, labs may not directly correlate with true electrolyte level. Therefore, continuous monitoring is essential to properly replete patients.
Satyendra Dhar MD, @DharSaty
#hypokalemia #hyponatremia #hypocalcemia #hypomagnesemia #hypophosphatemia #electrolytes
Lower Extremity Ulcers
Ulcers are defined as abnormal breaks in the skin or mucous membranes. General principles of management of LE ulcers include wound debridement, infection control, application of dressings, off-loading of localized pressure, & treatment of underlying conditions such as DM & PAD. Lifestyle changes (e.g., smoking cessation & dietary modifications) should also be made to help manage underlying diseases.
Satyendra Dhar MD, @DharSaty
#Arterialulcer; #Diabeticneuropathy; #Diabeticulcer; #Legulcer; #Peripheralarterydisease; #Venousinsufficiency; #Venousulcer; #Woundcare #DM
Creatine kinase (CK) is an intracellular enzyme present in skeletal muscle, myocardium & brain; smaller amounts in visceral tissues. Released after disruption of cell membranes due to hypoxia or other injury.
Sustained increases in these levels can be a sensitive indicator of underlying muscle damage.
CK may increase to as much as 30 times the upper limit within 24 hrs of strenuous physical activity, then slowly decline over next 7 days.
The definitive diagnosis of rhabdomyolysis is reliably made by serologic testing for creatine kinase (CK). Elevated levels of CK are the hallmark of rhabdomyolysis.
CK functions as an energy reservoir for ATP:
Creatine + ATP = creatine kinase + ADP (adenosine diphosphate).
CK has a half-life of 1.5 days; its level elevated in the first 12 hours, peaks during the first 3 days, and normalizes at around 5 days after injury.
CK level five times the upper limit of normal (≈1000 U/L), without apparent cardiac or brain injury, confirms the diagnosis.
Risk of developing AKI is usually low when the CK level is below 10,000 U/L.
AKI at lower levels of CK noted with coexisting conditions, such as sepsis, hypotension, or underlying CKD.
Myoglobin levels rise rapidly (within 3 hours) and peak prior to serum CK levels.
Myoglobin has a short half-life of 2 - 3 hours and is rapidly excreted by the kidneys.
Rapid and unpredictable metabolism makes serum myoglobin a less useful marker of muscle injury than CK, and is rarely used in assessing the risk of AKI.
Satyendra Dhar, MD, @DharSaty
#rhabdomyolysis #creatinekinase #CK #myoglobin
