====Interpreting Lab results==== |[[wiki:labs#CRP]] |[[wiki:labs#βHCG]] |[[wiki:labs#Lactate]]\\ [[wiki:labs#Lipase]] |[[wiki:labs#Procalcitonin]]\\ [[wiki:labs#Pro BNP]] |[[wiki:labs#Troponin]] |[[wiki:labs#VBG]] | ====Electrolytes==== ^Na⁺ |[[wiki:labs#hyponatraemia]]\\ [[wiki:labs#hypernatraemia]] | ^K⁺ |[[wiki:labs#hyperkalaemia]]\\ [[wiki:labs#hypokalaemia]] | ^Cl^- |[[wiki:labs:#hypochloraemia]] | ^Urea | | ^Creat |[[wiki:labs#creatinine|Creatinine]] | ^Glu | | ^corr Ca⁺⁺ |[[wiki:labs#hypercalcaemia]]\\ [[wiki:labs#hypocalcaemia]] | ^PO₄⁼ |[[wiki:labs#hypophosphataemia|hypo-phosphataemia]] | ===Creatinine=== *levels can be elevated due to non-renal failure causes *increased ingestion: big meat eaters, protein supplements *assay interference: DKA, fasting, hyper-lipidaemia, haemolysis and drugs eg. cephalosporins, barbiturates and some chemoRx *reduced tubular secretion: trimethoprim, H2 antagonists ===Kidney failure staging=== ^Stage ^eGFR\\ ml/min/1.73m²BSA ^description ^ACR (AlbCreat mg/mmol Ratio) is used to calculate the ‘A stage’ of CKD | ^1 |=90 |Normal |A1 – <3\\ A2 – 3-30\\ A3 – >30 | ^2 |60-89 |Mild |[{{:wiki:stages-of-kidney-disease_table.png?300|https://kidneyresearchuk.org/}}] | ^3a |45-59 |Mild Moderate |:::| ^3b |30-44 |Moderate |:::| ^4 |15-29 |Severe |:::| ^5 |<15 |Kidney Failure |:::| ===Hypercalcaemia=== *Primary hyperparathyroidism and malignancy are the two most common causes of increased serum calcium levels. If PTH levels are detectable, **//generally speaking//** the cause of hyper Ca++ is primary hyperparathyroidism *other causes include sarcoidosis, thyrotoxicosis *severe hypercalcaemia (>3.5 mmol/L) requires emergency management *can cause: *nephrogenic diabetes insipidus *abdo pain - constipation, ileus, pancreatitis *fatigue and even coma, Muscle weakness *Emergency Mx - IV saline, IV bisphosphonate if no success. *Other agents: calcitonin (100U SC per 6-8/24 or ≤10U/kg IV over 6/24 in emergency), dialysis, mithramycin and also anti-resorptive agent denosumab ===Hypocalcaemia=== *acquired or hereditary. Acquired causes include: *hypoparathyroidism *liver disease *kidney disease *pancreatitis, COVID-19 *hyperphosphataemia, hypomagnesaemia, vit D deficiency *diet, medication, and surgery ==Management== *Severe (ionized Ca⁺⁺ <1 mmol/L) - 10-20ml of 10% calcium gluconate over 10mins and repeated per hour until tetany, seizure or laryngospasm resolves *Without seizure or tetany: 10ml 10% over 1/24 *10ml of 10% solution (100mg/ml) = 1g = 2.2mmol ===Hypochloraemia=== *recurrent vomiting, gastric acid loss *diuretic-induced alkalosis (loop or thiazide diuretics) *posthypercapnic metabolic alkalosis. *CLD, cystic fibrosis, and laxative abuse are also potential causes. ===Hyperkalaemia=== *acute or chronic AKI/CKD *DKA *drug causes ^Mild |5.5-5.9mmol/L | ^moderate |6.0-6.5mmol/L | ^severe |>6.5mmol/L | ECG changes in rough order of appearance: {{ :wiki:pushpull-k-ecg.png?500|}} *Peaked T waves with a shortened QT interval *prolonged PR and QRS complex *disappearance of p wave *widening of QRS eventually progressing to a sine wave before asystole ==Management== |Stabilising the cardiac membrane with calcium ions. |10mL of 10% Ca⁺⁺ gluconate (=2.2mmol) or chloride (6.8mmol)\\ caution: bradycardia and arrhythmias | |Driving extracellular potassium into the cells |1. 10U actrapid, 50mL of 50% glucose\\ 2. Neb Salbutamol 20mg or IV 0.5mg\\ 3. HCO3- infusion - 1mmol/kg. ..if acidotic. Not useful on its own. Adjunct to #1&2 | |Removing excess potassium from the body |1. binders - **Sodium zirconium cyclosilicate** (Lokelma) 10g tds intially, action onset 1/24, Patiroma calcium 8.4g OD onset 4-7/24, Sodium polystyrene sulfonate (Resonium) 15g tds.\\ 2. Dialysis\\ 3. diuretics - mannitol, furosemide - theoretical but no trials to support | [[https://www.rqia.org.uk/RQIA/files/b0/b071ebc3-f2b3-48ab-8e46-c690df790177.pdf|rqia guidelines for Hyperkalaemia 2021]] ===Hypokalaemia=== *Increased GI losses *vomiting & diarrhoeal causes *bowel preps *tumour related - intestinal adenomas *Renal losses *Diuretics, amphotericin *hypomagnesaemia *renal tubular acidosis *other salt wasting nephropathies *Skin losses - sweating, CF, other skin conditions including burns *Dialysis and other transfusion related conditions *Chronic alcoholism *hyperaldosteronism *associated with [[wiki:endocrine:diabetic_ketoacidosis_dka|DKA]] **Requires treatment when severe - eg <2.5mmol/L or symptomatic** *severe muscle weakness, paralysis *DKA *cardiac arrhythmias ===Hypernatraemia=== *usually in elderly with mental or physical disability exacerbated by acute infection *as a result of impaired thirst or access to adequate water or increased losses *water losses - diuretics, osmotic diuresis (eg hyperglycaemia), acute tubular necrosis, GI losses and sweating ===Hyponatraemia=== *represents water excess *often related to loop diuretics but also associated with other disease processes which have been recognised to initiate [[wiki:endocrine:siadh|SIADH]] ===Hypophosphataemia=== *redistribution - associated with major surgery fluid shifts, insulin/glucagon/adrenaline use, respiratory alkalosis *beware esp in Rx of hyperglycaemia, DKA (osmotic losses + redistribution with insulin) *decreased absorption - malnutrition, alcohol Xs, anorexia *increased renal loss - associated with diuretics *renal replacement therapies - loss in effluent with large fluid shifts *//**Clinical**// - muscle weakness, CNS changes, poor WCC function reducing resistance to infection, arrhythmias *//**Treatment**// - depends on level *<0.64mmol/l & asymptomatic - preferably enteral replacement (Phosphate Sandoz tablets contain 500mg elemental phosphorous - 4-6 tablets daily for adults, 2-3 for kids) *<0.32mmol/l or symptomatic - parenteral replacement ====CRP==== C-reactive protein - increases with age and BMI *synthesised in liver in response to inflammatory stimuli, usually peaking in 2/7 *both pro and anti-inflammatory actions *exact mechanism of actin unknown but triggers complement pathway and others *also produced in endothelium, smooth M and adipose tissue *t_1/2 = 20/24 *raised in response to any inflammatory stimulus - infection (viral, TB, fungal etc), trauma, auto-immune diseases (Crohn disease, rheumatoid arthritis, juvenile idiopathic arthritis, vasculitis, autoimmune hepatitis), necrosis, ischaemia, malignancy etc *[[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5471098/|Causes and outcomes of markedly raised CPR 2017]] *high sensitivity CRP (hs-CRP) useful in high risk coronary disease ====Lactate=== |{{:wiki:lactate_pathway.png?300|}}|**Lactic acidosis** - Raised Lactate with pH≤7.35\\ **hyperlactaemia** - lactate >2 regardless of pH\\ elevated Lactate levels usually result from tissue hypo-perfusion or hypoxia.\\ **Consider:**\\ •shock, sepsis, anaemia\\ •malignancy, liver disease, DKA\\ •drugs - ß agonists, Metformin, paracetamol, cocaine | ====Lipase==== Lipase is found in most parts of the GI tract but has also has been found in liver, heart, lungs and leukocytes *acute pancreatitis usually associated with 2-3x rise in lipase *less significant rise in lipase associated with many illnesses *more specific than amylase for pancreatitis *significant increases in lipase (>3x upper limit) can be seen with: *reduced clearance of lipase caused by renal impairment or macrolipase formation *other hepatobiliary, gastroduodenal, intestinal and neoplastic causes *critical illness, including neurosurgical pathology *alternative pancreatic diagnoses, such as non-pathological pancreatic hyperenzymaemia *miscellaneous causes such as diabetes, drugs and infections. (esp. Narcotics, thiazide diuretics, oral contraceptives, adrenocorticotropic hormone, cholinergics but many others as well have been associated with rise) *Multi trauma without head injury can also cause 3x rise in lipase [[https://www.ncbi.nlm.nih.g ov/pmc/articles/PMC4299384/|non pancreatic causes of raised lipase]]\\ ====βHCG==== *considerable variation but 50% women will have values as below within 3/7 of value shown *tend to plateau and begin to decline around d60 (ie. ~9/40) [[http://pathology.royalberkshire.nhs.uk/HCGrange.php]] ^HCG ^day post LMP | |42 |24 | |53 |25 | |67 |26 | |85 |27 | |113 |28 | |150 |29 | |200 |30 | |267 |31 | |350 |32 | |450 |33 | |592 |34 | |784 |35 | |1084 |36 | |1418 |37 | |1918 |38 | |2586 |39 | |3587 |40 | |5171 |41 | |6840 |42 | |9175 |43 | |11677 |44 | |15014 |45 | |19184 |46 | |23355 |47 | |28359 |48 | |33364 |49 | |38369 |50 | |42539 |51 | |46710 |52 | |51714 |53 | |56719 |54 | |61723 |55 | |66728 |56 | |71733 |57 | |75903 |58 | |80074 |59 | |84244 |60 | ====Pro BNP==== [[https://core.ac.uk/download/pdf/160755318.pdf|ProBNP in the ED, AmCollege of Cardiology 2018]]\\ ====Procalcitonin=== *Practically all PCT formed in thyroid C cells is converted to calcitonin so that no PCT is released into the circulation. Hence, the PCT level in healthy subjects is very low (0.05 ng/mL) *inflammatory release of PCT is independent. During inflammation, PCT is produced mainly by two alternative mechanisms; direct pathway induced by lipopolysaccharide (LPS) or other toxic metabolite from microbes and indirect pathway induced by various inflammatory mediators like IL-6, TNF-a, etc *PCT is generally elevated by bacterial infection but not viral *not usually raised with PE and therefore may be useful in differentiating pneumonia and PE particularly when associated with fever {{:wiki:pct_sepsis.jpg?400|}} ====Troponin==== *patients with a 5 mL/min/1.73 m2 lower mean eGFR had 13% higher levels of mean hs‐cTnT. *patients with pre-existing CHF had a 34% higher level of hs‐cTnT, history of hypertension (34%), myocardial infarct (33%), angina pectoris (31%), atrial fibrillation (26%), of male sex (24%), diabetes mellitus (24%), and patients with lower hemoglobin (4% per 10 g/L). *reason for raised Trop is unclear in CKD - may be related to reduced clearance although small molecules are able to pass through glomerular membrane. May be due to chronic stress assoc with CKD [[https://www.ahajournals.org/doi/10.1161/JAHA.119.013091|Assoc b/w Troponin and renal function - AHA 2019]]\\ troponin is known to rise post neurological insult eg. SAH, but is also associated with seizures [[https://www.seizure-journal.com/article/S1059-1311(20)30165-5/fulltext#secsect0005|ESocJ seizures]] ====VBG==== **Venous Blood Gas** | ^ how it compares with ABG ^art ^venous | ^pH |• good correlation |7.35-7.45 |7.31-7.41 | ^pO2 |• poor correlation\\ • useful in tracking change |10.6-13.3 |4.0-5.3 | ^pCO2 |• good correlation usually\\ • poor in severe shock and worsens with higher values |4.7-6.0 |5.5-6.8 | ^HCO3 |• good correlation |22-28 |23-29 | ^Lactate |• good correlation at 1st but worsens as levels increase ||| ^Base Excess |• good correlation ||| ====Full Blood Exam==== ^Hb || ^WCC |aside from infection, acute rise in trauma, pregnancy\\ | ^PMN || ^Platelets |thrombocytopaenia, [[wiki:labs#thrombocytosis]] | ====Thrombocytosis==== **//Thrombocythemia//** - high platelet count that is not caused by another health condition. AKA primary or essential thrombocythemia.\\ **//Thrombocytosis//** - high platelet count secondary to other disease or condition. AKA secondary or reactive thrombocytosis. More common than thrombocythemia. **Thrombocytosis** *Anemia: Iron-deficiency anemia and hemolytic anemia *Cancer - esp lung, gastrointestinal, breast, or ovarian cancer or lymphoma.Occasionally is first sign of cancer. *Splenectomy: stores platelets. Removing your spleen can raise your platelet count. *Inflammation/infections - eg. connective tissue disorders, inflammatory bowel disease, and tuberculosis ====Erythrocyte Sedimentation Rate (ESR)==== [[https://www.ncbi.nlm.nih.gov/books/NBK557485/|ESR review 2021]]\\ *The Westergren method measures the distance (in millimeters) at which red blood cells in anticoagulated whole blood fall to the bottom of a standardized, upright, elongated tube over one hour due to the influence of gravity *useful, but not specific, to monitor many inflammatory disease processes *typically higher in females, and increases with age *Polycythaemia, spherocytosis and sickle cell may **lower ESR** *extreme elevation seen in: infection, collagen vascular disease, metastatic disease ^ Clotting ||| ^PT ^APTT | | ^prolonged ^normal |Factor VII deficiency\\ Mild vitamin K deficiency\\ Liver disease\\ Warfarin (can prolong both in higher doses\\ DIC | ^normal ^prolonged |Deficiency of factor VIII, IX, or XI\\ Deficiency of factor XII, prekallikrein, or HMW kininogen (not associated with a bleeding diathesis)\\ von Willebrand disease (variable)\\ Heparin, dabigatran, argatroban, direct factor Xa inhibitors (variable)\\ Acquired inhibitor of factor VIII, IX, XI, or XII\\ Acquired von Willebrand syndrome\\ Lupus anticoagulant (more likely to be associated with thrombosis than bleeding) | ^prolonged ^prolonged |Deficiency of prothrombin, fibrinogen, factor V, or factor X\\ Combined factor deficiencies\\ Liver disease\\ DIC\\ Severe vitamin K deficiency\\ Anticoagulants (supratherapeutic doses of many anticoagulants, combined heparin and warfarin, direct thrombin inhibitors, anticoagulant rodenticide poisoning)\\ Acquired inhibitor of prothrombin, fibrinogen, factor V, or factor X\\ Amyloidosis-associated factor X deficiency| | | |Warfarin typically prolongs the PT alone, but at high levels warfarin can prolong both tests.\\ Heparin typically prolongs the aPTT alone (because PT reagents contain heparin-binding agents that block heparin effect), but at high levels heparin can prolong both tests.\\ Direct thrombin inhibitors (argatroban, dabigatran) typically prolong both tests, but at low levels dabigatran may not prolong the PT.\\ Direct factor Xa inhibitors (apixaban, edoxaban, rivaroxaban) can prolong the PT and aPTT, although these effects are variable.\\ [[https://www.uptodate.com/contents/image?imageKey=HEME%2F79969&topicKey=HEME%2F1333&source=see_link|UpToDate]]| ^INR | |**Major bleeding in patients on warfarin** (in combination with dried prothrombin complex or fresh frozen plasma) for phytomenadione\\ By slow intravenous injection - Adult\\ 5 mg for 1 dose, stop warfarin treatment.\\ **INR > 8.0 with minor bleeding in patients on warfarin** for phytomenadione, by slow IV - Adult\\ 1–3 mg, stop warfarin treatment, dose may be repeated if INR still too high after 24 hours, restart warfarin treatment when INR <5.\\ **INR > 8.0 with no bleeding in patients on warfarin** for phytomenadione by mouth - Adult\\ 1–5 mg, IV preparation to be used orally, stop warfarin treatment, repeat dose if INR still too high after 24 hours, restart warfarin treatment when INR <5.\\ **INR 5.0–8.0 with minor bleeding in patients on warfarin** for phytomenadione by slow IV injection - Adult\\ 1–3 mg, stop warfarin treatment, restart warfarin treatment when INR <5. | ===d-Dimer=== *raised d-Dimer needs to be interpreted in context and VTE can be found despite a -ve d-Dimer result eg. small or matured clots or in patients with deranged fibrinolysis eg Factor XIII def. *Often raised in conditions other than 'pure' VTE: *60% older patients have d-Dimer value higher than classical cutoff. An age related formula is useful for patients >50y: Age (years) x 10 µg/L *trauma *upper GI haemorrhage and liver disease *stroke *ACS, AF, lipaemia *consumptive coagulopathy - [[wiki:haematology:DIC]], VICC (venom induced consumptive coagulopathy) *later stages of pregnancy & pre-eclampsia *inflammatory disorders, malignancy, sickle cell disease *often raised in elderly and , cigarette smokers, Afro-Americans, post-op *Afro-Caribbean patients, especially women, typically have much higher d-Dimer levels. However, also associated with other co-morbidities and poor outcomes [[https://onlinelibrary.wiley.com/doi/full/10.1111/j.1538-7836.2008.03215.x|J of thrombosis & haemostasis - dDimer and ethnicity]]\\ [[https://academic.oup.com/biomedgerontology/article/55/11/M649/563341#8995638|J of Gerontology - dDimer and age, functional status etc]]\\ d-Dimer in PREGNANCY: For pregnant women, the following D-Dimer reference value ranges are proposed: [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7273490/|dDimer in pregnancy]] ***1st trimester:** 167-721 ng/mL ***2nd trimester:** 298-1653 ng/mL ***3rd trimester:** 483-2256 ng/mL fibrinogen in pregnancy: *1st trimester: 2.64-6.56 g/L *2nd trimester: 3.40-8.53 g/L *3rd trimester: 3.63-9.14 g/L. d-Dimer in LIVER DISEASE: *[[https://www.spandidos-publications.com/10.3892/etm.2016.3930]] *Infection: typically raised with [[wiki:respiratory:infections#lower_respiratory_infection|CAP]] according to severity. Using **Pneumonia Severity Score** {{popup>:wiki:respiratory:pneumoniaseverityindex.png?200 |(PSI)}}: ^dDimer varies with PSI | | ^Group 1 |~190 | ^Group 2 |~320 | ^Group 3 |~470 | ^Group 4 |~660 | ^Group 5 |~1230 | *'rule out' for imaging etc still requires using [[wiki:respiratory:pulmonaryembolism#wells_criteria|Wells]] or other clinical criteria (View Cascade)<@anno:[1;;anno_dylan]>{{:wiki:haematology:coagulation_cascade.png.jpg?400|}} ====Liver function tests==== ^AST |• raised in proportion to cellular damage and especially early stage of necrosis\\ • found in cardiac and skeletal M, kidney, brain, pancreas and red cells and therefore ??? in skeletal M trauma and other Muscle disorders, MI, hepatitis etc | ^ALT |• levels not related to degree of liver necrosis and not useful in prognosis\\ • more specific than AST for liver damage\\ • higher levels seen with chronic hepatitis, cholestasis, CCF, infectious mononucleosis, various drugs eg paracetamol, phenothiazines, barbiturates, morphine, tetracyclines\\ • isolated elevated ALT - consider rechecking in >6/12. If remains high - then Ix for hepatocellular disease\\ • remember that 'normal' range is just that - Bell curve means that 2.5% pop will be outside 'normal' range | ^AST:ALT <1 |• viral hepatitis\\ • severe toxic hepatitis\\ • ischaemic hepatitis | ^AST:ALT >2.5 |• classic alcoholic liver disease with acute hepatocellular injury\\ • active cirrhosis | ^ALP |• primarily biliary stasis/obstruction and malignancy\\ • also a marker of bone turnover and therefore seen with bony disorders & metastases\\ • normally high in late pregnancy | ^dGT |• sensitive to alcohol ingestion and especially with biliary obstruction\\ • also raised in pancreatitis, brain tumours, renal and prostatic disease and post MI | ^LDH |• found in most tissues\\ • especially raised in CCF, PE's and infarction, anaemias, hepatitis\\ [[https://www.ncbi.nlm.nih.gov/books/NBK557536/|StatPearls 2021 LDH biochem]] | ^ Summary of enzyme patterns in Liver Disease ^|||||| ^ ^ ALP ^ AST ^ ALT ^ dGT ^ //**other**// | ^Cholestasis | ↑↑ | ↑ | ↑ | ↑↑ |AST:ALT<1.5 suggests extrahepatic, >1.5 suggests intrahepatic | ^Prim Biliary Cirrhosis | ↑↑↑ | ↑/N | ↑/N | ↑↑ |raised AST:ALT suggests cirrhosis | ^Prim sclerosing cholangitis | ↑↑ | ↑/N | ↑/N | ↑↑ |AST:ALT>1 may suggest cirrhosis\\ >1.12 suggests risk of varices | ^Alcoholic Liver Disease | ↑/N | ↑ | ↑ | ↑↑ |AST:ALT>2 | ^NAFLD/NASH |↑/N | ↑ | ↑ | ↑ |AST:ALT<1 unless cirrhosis | ^Wilsons disease | ↑ | ↑↑ | ↑↑ | ↑ |ALP:bili<4, AST:ALT>2.2 | ^Hep B, C | ↑ | ↑↑/N | ↑↑/N | ↑ |AST:ALT>1 suggests cirrhosis\\ AST:platelets>1.5 suggests moderate fibrosis\\ enzymes may all be N | ^Autoimmune Hepatitis | ↑ | ↑↑ | ↑↑ | ↑ |persistently high transaminases suggests poor prognosis | ^Ischaemic/shock injury\\ Toxic injury | ↑ | ↑↑↑ | ↑↑↑ | ↑ | | ===vit B12=== [[https://academic.oup.com/qjmed/article/106/6/505/1538806|Elevated B12 in clinical practice - review 2013]]\\ paradoxically accompanied by signs of deficiency, - a functional deficiency linked to qualitative abnormalities,eg. defects in tissue uptake and action of vitamin B12 high levels not infrequently associated with solid tumours: *myeloproliferative blood disorders * hepatocellular carcinoma (HCC) and secondary liver tumours *breast cancer, colon cancer, cancer of the stomach and pancreatic tumours. ==References include:== [[https://emj.bmj.com/content/20/4/319|BMJ role of fibrin dDimer in Emerg Med 2003]]\\ https://rebelem.com/age-adjusted-d-dimer-testing/\\ https://litfl.com/dealing-with-d-dimer-debacles/\\ [[https://www.lesjeudisdefleurus.org/uploads/files/page/D-dim%C3%A8res_J_Favresse.pdf|dDimer variables, uses, production]]\\ https://litfl.com/liver-function-tests/\\ [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3609680/|Function of Liver function tests 2012]]\\ [[https://bestpractice.bmj.com/topics/en-gb/59|assessment of hypokalaemia 2020]]\\ [[https://emedicine.medscape.com/article/2086909-overview#a4|emed review of CRP]]\\ [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3826426/|CRP interpretation in critically ill 2013]]\\ [[http://www.dickyricky.com/Medicine/Papers/2019_08_29%20Ann%20Emerg%20Med%20Demystifying%20Lactate%20in%20the%20Emergency%20Department.pdf|Lactate in ED 2019]]\\ [[https://www.westsuffolkccg.nhs.uk/wp-content/uploads/2013/01/ALT-pathway-final1.pdf|Suffolk ALT pathway]]\\ [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297576/|RCP hypercalcaemia - presentation and Mx 2017]]\\ [[https://www.endocrinologyadvisor.com/home/decision-support-in-medicine/endocrinology-metabolism/tumor-induced-hypercalcemia/|Endocrinology Advisor- Hypercalcaemia]]\\ [[https://bjaed.org/article/S1743-1816(17)30386-4/pdf|Brit J An: Lactate in Health & Disease]]\\ [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3383162/|False estimates Creat]]\\ [[https://bjaed.org/article/S2058-5349(17)30041-0/pdf|Phosphate homeostasis in Critical Care 2016]]\\ [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898550/#:~:text=CONCLUSIONS%3A,normally%20cause%20such%20an%20increase.|dDimer and CAP review ]]\\ [[https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5543591/|Procalcitonin as Dx marker of sepsis. J Int Care 2017]]\\