AKI CME EDIT management,clinical features and presentation

AKI management

1. ACUTE KIDNEY INJURY PRESENTERS : DR.JUWAN MBABAZI FIONAH DR.KASUMBA UMAR SUPERVISOR: DR.AJOK BRENDA (PYSICIAN)

2. OUTLINE CASE PRESENTATION 2 CASE DISCUSSION 3 REACTIONS

3. CASE PRESENTATION BIODATA NAME: N. A AGE:76YEARS SEX:FEMALE ADDRESS: KABULANAKA DOA:20/02/2024 DATE OF DISCHARGE:28/02/2024

4. CASE PRESENTATION CONTINUED.. PRESENTING COMPLAINT Reduced level of consciousness for 1day

5. CASE PRESENTATION CONTINUED.. 76/F known HTN being managed on LOSARTAN H AND AMLODIPINE was well till one day prior to admission when caretakers reported a history of a sudden fall, the fall was associated with confusion and disorientation in place however reported no visible injuries and a few hours later the patient got better. 2 hours prior to admission the patient lost consciousness this was associated with tonic clonic convulsions that lasted approximately 4 minutes however there was no history of neck stiffness, no photophobias, no slurring of speech and no focal neurological deficits

6. CASE PRESENTATION CONTINUED.. REVIEW OF OTHER SYSTEMS She reported history of cough associated with chest pain and difficulty in breathing Other systems were unremarkable

7. CASE PRESENTATION PMHX : has had hypertension for 2years ON EXAMINATION Eldery lady, unconscious, GCS 12/15(E:3,V:4,M:5) Blood pressure 133/66 mmhg saturation 72%, Random blood glucose: ERROR 8

8. CASE PRESENTATION RESPIRATORTY EXAM Noted bilateral basal crackles AND ALL THE OTHER SYSTEMS WERE NORMAL

9. INVESTIGATIONS Malaria blood smear…..1-2mps Rbs after 2 hours of n/s….26mmol/l Serum electrolytes….. hypernatremia,hyperkalemia Cbc …. neutrophilia RFTs…urea 552.60 increased 13 times the upper limit), creatinine 5.57(increased 5 times the upper limit) lfts … ast 78.789 slightly increased) URINALYSIS…no ketones,glycosuria RCT…NEGATIVE

10. DIAGNOSIS 76/F KNOWN HYPERTENSIVE WITH; MALARIA SEVERE PNEUMONIA NEWLY DIAGONISED DM TYPE 2 WITH HHS ACUTE KIDNEY INJURY ELETROLYTE IMBALANCE

11. MANAGEMENT PLAN Oxygen therapy at 5litre/minute. IV normal saline 2litres stat for the first two hours Iv ceftriaxone 2g stat Monitor urine output Administer short acting insulin using a sliding scale Do ct scan Review by nephrologist

12. management Day two; Patient continued to be disoriented and had reduced levels of consciousness rbs was 11.7 mmol /hence patient was fixed on mixtard Continued maintainance fluids,iv ABX patient was reffered for ctscan of the brain

13. case DAY THREE; PATIENT WAS CONSCIOUS WITH A GCS OF 15/15 noted normal ct scan. REPEATED RFTS and Lfts which were near normal Patient was reviewed by a nephrologist who recommended to discontinue glibenclamide and tbs metformin

14. The next few days were spent treating severe pneumonia and later patient was discharged on 8 th admission day

15. Definition AKI Acute kidney injury previously called ARF AKI is defined as an abrupt (within hours) decrease in kidney function, which encompasses both injury (structural damage) and impairment (loss of function). Diagnostic approach of AKI is based on an acute decrease of GFR, as reflected by an acute rise in sCr levels and/or a decline in UO over a given time interval sCr marker of GFR

16. Cont. Principal tools to detect AKI were consecutive measurements of sCr , serum urea ( sUr ), urinalysis, and measurements of UO. 2 Defination of AKI Acute Kidney Injury Network (AKIN) RIFLE criteria KDIGO (Kidney Disease Improving Global Outcomes),

17. AKI, as defined by RIFLE

18. KDIGO definition, AKI is absolute increase in sCr , at least 0.3 mg/ dL (26.5 µ mol /L) within 48 hours or by a 50% increase in sCr from baseline within 7 days, or a urine volume of less than 0.5 mL/kg/h for at least 6 hours

19. KDIGO Defination

20. Epidemiology Hospital inpatients it is estimated to occur up to 15% and is more common in critically ill patients, in whom its prevalence is estimated to be up to 60% Accounts for 4.3% among all hospital admission ( Konstantinos m et al , 2016) 1 in 5 adults & 1 in 3 children in developing countries ( Oleksa et al, 2019)

21. ETIOLOGY PRERENAL INTRISIC POST RENAL

22. PRERENAL Most common form of AKI Approximately 1200ml of blood or 25% of cardiac output flows through the kidney every minute

23. PRERENAL CONTINUED GFR is reduced due to decreased perfusion pressure to the kidney By definition, involves no parenchymal damage to the kidney Rapidly reversible once intraglomerular hemodynamics are restored

24. PRERENAL AKI Volume depletion Renal losses (diuretics, polyuria) GI losses (vomiting, diarrhea) Cutaneous losses (burns, Stevens-Johnson syndrome) Hemorrhage Pancreatitis Decreased cardiac output   Heart failure Pulmonary embolus Acute myocardial infarction Severe valvular heart disease Abdominal compartment syndrome (tense ascites)

25. INTRISIC CAUSES Glomerular   Anti–glomerular basement membrane (GBM) disease ( Goodpasture syndrome) Anti–neutrophil cytoplasmic antibody-associated glomerulonephritis (ANCA-associated GN) (Wegener granulomatosis , Churg -Strauss syndrome, microscopic polyangiitis ) Immune complex GN (lupus, postinfectious , cryoglobulinemia , primary membranoproliferative glomerulonephritis) Tubular Ischemi Toxic Heme pigment ( rhabdomyolysis , intravascular hemolysis) Crystals (tumor lysis syndrome, seizures, ethylene glycol poisoning, megadose vitamin C, acyclovir, indinavir , methotrexate) Drugs (aminoglycosides, lithium, amphotericin B, pentamidine , cisplatin , ifosfamide , radiocontrast agents

26. POST RENAL Ureteric obstruction Stone disease, Tumor, Fibrosis, Ligation during pelvic surgery Bladder neck obstruction Benign prostatic hypertrophy [BPH] Cancer of the prostate Neurogenic bladder Drugs(Tricyclic antidepressants, ganglion blockers, Bladder tumor, Stone disease, hemorrhage/clot) Urethral obstruction (strictures, tumor)

27. CLINICAL MANIFESTATIONS Symptoms: Fever, rash, joint pains, myalgias Concern for SLE, vasculitis , acute interstitial nephritis. Dyspnea – heart failure. Hemoptysis – Goodpasture’s , Wegener’s. Preceding bloody diarrhea – HUS. Preceding pharyngitis – post-Strep GN, post-infectious GN.

28. Pathophysiology Decreased renal blood flow stimulates salt and water retention to restore vol. and pressure. When Volume or Pressure is decreased, the baroreceptors receptors reflexes located in Aortic arch and Carotid sinus are activated→symphat nn activation →renal afferent arteriolar vasoconstriction & renin secretion thru ℬ1receptor.

29. Pathophysiology cont Constriction of the afferent arterioles causes a decrease in intraglomerular pressure which reduces GFR. Renin converts Angiotensin 1 to 11,which stimulates Aldosterone release→ salt and water absorption in the distal collecting tubules. A decrease in vol. or pressure is a non osmotic stimulus for Hypothalamic production of ADH →H2O reabsorption

30. Pathophysiology Thru unknown mechanism, activation of SNS→enhanced prox. tubular reabsorption of salt & water as well as BUN,Cr,Uric acid, HCO3 The net effect of these mechanism is decreased output and decreased urinary excretion of Sodium

31. Treatment and management of AKI The current treatment for AKI is mainly supportive. Maintenance of volume homeostasis and correction of biochemical abnormalities are the primary goals of treatment and may include; Correction of fluid overload with furosemide Correction of severe acidosis with bicarbonate administration Correction of hyperkalemia Correction of hematologic abnormalities e.g. anemia, uremic platelet dysfunction, with transfusions and administration of desmopressin or estrogens

32. VOLUME OVERLOAD Furosemide can be used to correct volume overload when kidneys are still responsive. However, it plays no role in converting oliguric AKI to a non oliguric AKI, or increasing urine output in hypovolemic patient. Match fluid intake to urine output plus an additional 500 mL to cover insensible losses once patient is euvolaemic Correct hypovolaemia and optimize systemic hemodynamic status with inotropic drugs if necessary e.g. noradrenaline ( this improves microcirculatory flow by increasing perfusion pressure above the auto regulation threshold inhypotensive patients) vasopressin, terlipressin . If MAP is less than 65mmHg, to maintain renal perfusion.

33. PULMONARY EDEMA Sit the patient up, give high flow oxygen IV furosemide infusion 100-250mg at 4mg/min Consider salt and fluid restriction e.g. 0.75 – 1.0l/day

34. TREATMENT OF HYPERKALEMIA If the objective therapy is to; Stabilize cell membrane potential IV calcium gluconate (10 mL of 10% solution) Shift K into cells Inhaled β2- adrenoceptor agonist (e.g. salbutamol) IV glucose (50 mL of 50% solution) and insulin (5 U Actrapid ®) IV sodium bicarbonate2 Remove K from body IV furosemide and normal saline Ion-exchange potassium binding resin (e.g. Resonium ) across gut lumen orally or rectally Dialysis

35. NEPHROTOXIC AGENTS • Discontinue potentially nephrotoxic drugs and reduce doses of therapeutic drugs according to level of renal function e.g. NSAIDS, ARBs ACEI, Metformin, aminoglycosides, vancomycin

36. CONT. Ensure adequate nutritional support Administer proton pump antagonists to reduce the risk of upper gastrointestinal bleeding Screen for intercurrent infections and treat promptly if present

37. INDICATIONS OF RRT Severe or refractory hyperkalemia Severe or refractory metabolic acidosis Refractory fluid overload Clinical complications of uremia (azotemia) e.g. encephalopathy, pericarditis or neuropathy Anuria NB; RRT should be initiated within 8hrs of fulfilling KDIGO stage 2 of AKI.

38. PROGNOSIS There is an increased risk of CKD and ESKD among patients that recover from in hospital AKI with albuminuria, lower baseline eGFR , old age, female sex, higher creatinine at discharge, other comorbidities like heart failure, DM, HTN