![Management of Hypertensive Crisis / Encephalopathy
1. Intravenous Sodium Nitroprusside [Arterial & venous vasodilator]
Dose : 0.3 µg / kg / min (max 10 µg / kg / min)
2. Propranalol: [b 1 selective blocker]
Dose: 1-3 mg / kg / dose q 12 h
3. Esmolol: [b 1 selective blocker]
Dose: 130 – 300 µg / kg / min
4. Nifidepine: (Calcium channel blocker)
Dose : 0.5 mg / kg Sublingual repeated after 30 min
5. Amlodepine:(Calcium channel blocker)
Dose : 0.1 to 0.6 mg / kg / d in 2-3 doses – Oral
6. Labetelol: [Combined b -adrenergic (b1 & b2) and a-adrenergic blocker] Dose :
0.2-1.0 mg/kg can be given as an IV bolus every 10 min; Dosages of 0.25 - 3
mg / kg / hr by IV infusion..
7. Hydralazine: [Direct arterial vasodilator with no effect on venous circulation]
Dose : 0.1 - 0.2 mg / kg every 2 hrs (max 10 µg / kg / min)](https://image.slidesharecdn.com/agn-250129194736-516f0a57/85/AGN-pptx7777777777777777777777777777777777777777777-35-320.jpg)
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- 2. Acute Glomerulonephritis PRESENTED BY: MOHAMED LAHAI MARRAH………………….22065 ABDULAI M.S. MANSARAY…………………….22063
- 3. CONTENT • Introduction • Definition • Incidence • Etiology • Pathophysiology • Clinical manifestations • Diagnostic evaluations
- 4. CON’t • Management • Complications • Prevention • Conclusion
- 5. Acute glomerulonephritis is a common disease in children and it is one of the disease that are presented commonly with hematuria. Acute glomerulonephritis can result in long- term damage or may resolve, depending upon the cause and severity. Introduction
- 6. Definition • An acute inflammation of renal glomerular parenchyma due to deposition of immune complexes characterized by sudden onset of oliguria, hematuria, hypertension and edema
- 7. Incidence • Its account for pediatric admissions in the world about 1% to 5% • 90 % of renal disease in childhood
- 8. Aetiology Classification 1:Primary glomerulonephritis 1- Immune complex glomerulonephritis: - Post infectious glomerulonephritis: May follow infection with Strept, Staph, Pneumococci, HBV, Echo, Coxachie. - Membranoproliferative glomerulonephritis (MPGN). - lgA Nephropathy (Berger's disease),measles,mumps,varicella,syphilis,typhoid,meningococcal infections. 2- Anti glomerular basement membrane glomerulonephritis (Good-Pasteur syndrome). 3- Uncertain cause e.g. Focal segmental glomerulonephritis. 2:Glomerulonephritis with systemic disorders: 1- Immune mediated: - Lupus nephritis. - Henoch Shonlein purpura. 2- Heriditary e.g. - Alport syndrome.
- 10. Electron microscopy, electron-dense deposits, or “humps,” are observed on the epithelial side of the glomerular basement membrane Immunofluorescence microscopy :- pattern of “lumpy-bumpy” deposits of immunoglobulin and complement on the glomerular basement membrane and in the mesangium.
- 11. Pathophysiology • The pathophysiology of acute glomerulonephritis (AGN) involves immune-mediated damage to the glomeruli, leading to inflammation and impaired kidney function. AGN can be triggered by infections, autoimmune diseases, or systemic conditions, each initiating a series of immune responses that damage the glomerular capillaries. Here’s a breakdown of the main steps in AGN pathophysiology:
- 13. Clinical Manifestations Hematuria: Due to capillary damage, red blood cells leak into the urine, causing hematuria (often with red blood cell casts). Proteinuria: Glomerular damage also leads to the leakage of proteins, though typically less severe than in nephrotic syndrome. Oliguria: Reduced GFR results in decreased urine output (oliguria).
- 14. Hypertension: Fluid retention and activation of the renin- angiotensin-aldosterone system (RAAS) due to kidney hypoperfusion lead to elevated blood pressure. Edema: Sodium and water retention contribute to edema, particularly around the eyes and in the legs.
- 15. Acute Post Streptococcal Glomerulonephritis • Definition: Acute Nephritic syndrome which follow infection with nephritogenic strain of group A-{3 hemolytic streptococci (serotypes 4, 12 causing throat infection or serotypes 49 causing skin infection).
- 16. Post Streptococcal Glomerulonephritis • Streptococcal serotypes involved • Pharyngitis : • Types 1,4, 5, 12, 25 • Pyoderma • Types 49, 55, 57, 60 • Streptococcal antigens involved in immune response Usually occurs 7-14 days after pharyngitis and 2 wks – 6 wks after skin infection
- 17. Post Streptococcal Glomerulonephritis RISK FACTORS Age group 2 – 12 yrs (Rare before 2 yrs) Sex Male predominance Socioeconomic group Common in low socioeconomic group Seasonal variation During winter and rainy season serotype 12 causes Ac. pharyngitis During summer – serotype 49 causes skin infections
- 18. Pathogenesis • The pathogenesis of post-streptococcal glomerulonephritis (PSGN) involves an immune response triggered by a preceding streptococcal infection. This response results in inflammation and damage to the kidney’s glomeruli. Here's a step-by-step outline of the process:
- 19. Initial Streptococcal Infection PSGN typically occurs after a throat or skin infection caused by group A beta-hemolytic Streptococcus (Streptococcus pyogenes).The infection often occurs 1–3 weeks before the onset of glomerulonephritis symptoms.
- 20. Immune Complex Formation During the infection, the immune system produces antibodies against streptococcal antigens.Some streptococcal antigens (e.g., nephritogenic antigens like streptococcal pyrogenic exotoxin B ,Nephritis- associated plasma receptors( SPEB or NAPlr) may enter the bloodstream and reach the kidneys, or they may mimic certain kidney components.Antibodies bind to these antigens, forming immune complexes.
- 21. Deposition in Glomeruli These immune complexes are deposited in the glomeruli, the filtering units of the kidneys.The deposits typically occur in the glomerular basement membrane and mesangium.
- 22. Complement Activation and Inflammation the deposited immune complexes activate the complement system, leading to inflammation. Complement activation releases chemotactic factors that attract inflammatory cells (e.g., neutrophils) to the glomeruli. The inflammatory response damages the glomerular capillary walls, leading to a leakage of blood cells and proteins into the urine.
- 23. Post Streptococcal Glomerulonephritis Clinical Features • Puffiness of face – more in the mornings • Edema feet • Oliguria ( < 400 ml / m2 ) • Hematuria (cola coloured urine) • Breathlessness due to hypertensive heart failure • Fever • Hypertension • Abdominal pain • Atypical presentations: • Hypertensive encephalopathy – confusion, convulsions, etc. • Pulomonary edema – due to CHF • Acute renal failure
- 24. Post Streptococcal Glomerulonephritis Diagnostic criteria of APSGN At least 2 of the following criteria must be present 1. Positive throat or skin culture for streptococcus – Confirmatory or Carrier state 2. Streptococcal products like anti-streptokinase, anti- hyalironidase, anti-DNAse B, ASO titre are elevated (Anti – DNAse B is the single most specific test for Streptococcal infection) 3. Hypocomplementemia : Serum C3 reduced to 90% and CH50 decreased with in 2 weeks, but C4 is normal. • The antistreptolysin O titre is commonly elevated after a pharyngeal infection but rarely increases after streptococcal skin infections.
- 25. History taking & examinations urinalysis Serological tests Kidney biopsy Blood tests Throat swab culture Diagnostic Evaluation
- 26. Post Streptococcal Glomerulonephritis Investigations - For kidney injury : Urine analysis • Proteinuria – non selective; 1+ or 2+ protein with red cells • Hematuria : - Macroscopic: Plenty of RBC & RBC casts in urine - Microscopic: > 5 RBC / HPF in 10 ml centrifuged urine • Hypocomplementemia Kidney function Tests • Blood urea • S. creatinine (h due to i GFR)
- 27. Post Streptococcal Glomerulonephritis Course • Renal Failure – less than 1 % in children, slightly higher in adults • Resolution usually quick, • plasma Cr usually returns to previous levels by 3-4 weeks • Hematuria resolves usually within 3-6 months, • Proteinuria falls at a slower rate • Some patients experience htn, recurrent proteinuria, and renal insufficiency 10-40 yrs after • > 20% of adults may have some degree of persistent proteinuria and or compromise of GFR for 1 year
- 28. Post Streptococcal Glomerulonephritis Complications 1. Hypertensive encephalopathy Failure of autoregulatory system of the vessels of brain due to acute rise of blood pressure • Altered sensorium, convulsions, etc, 2. Hypertensive heart failure 3. Hypocalcemia 4. Hyperphosphatemia 5. Hyperkalemia 6. Acute renal failure 7.Pulmonary edema
- 29. 01 02 03 04 05 Diuretics Infections control Diet / fluids Tt of Hypertension Management of Complications Post Streptococcal Glomerulonephritis Management
- 30. Post Streptococcal Glomerulonephritis Management 1. Diet / fluids 2. Diuretics 3. Treatment of Hypertension 4. Infections control 5. Management of Lt ventricular failure
- 31. Diet / Fluids • Intake of sodium, potassium and fluids is restricted until blood levels of creatinine reduce and urine output increases • Overhydration may increase the risk of hypertension and precipitate left ventricular failure. • Monitor fluid Input and Output. Restriction of fluid intake to an amount equal to insensible losses and 24 hr urine output. • Daily weight monitoring 01
- 32. Diuretics: Treatment of Edema • For milder edema: Oral frusemide at a dose of 1-3 mg/kg; • For pulmonary edema: IV frusemide (2-4 mg/kg) The edema disappears with the return of renal function 02
- 33. Treatment of Hypertension • Mild cases – Managed with salt & water restriction. • Drugs used: • Atenelol, hydralazine, nifedipine, Risk of hyperkalemia with ACE inhibitors and beta blocker 03
- 34. Infections control If active pharyngitis or pyoderma is present Drug of choice: Penicillin for a period of 10 days 04
- 35. Management of Hypertensive Crisis / Encephalopathy 1. Intravenous Sodium Nitroprusside [Arterial & venous vasodilator] Dose : 0.3 µg / kg / min (max 10 µg / kg / min) 2. Propranalol: [b 1 selective blocker] Dose: 1-3 mg / kg / dose q 12 h 3. Esmolol: [b 1 selective blocker] Dose: 130 – 300 µg / kg / min 4. Nifidepine: (Calcium channel blocker) Dose : 0.5 mg / kg Sublingual repeated after 30 min 5. Amlodepine:(Calcium channel blocker) Dose : 0.1 to 0.6 mg / kg / d in 2-3 doses – Oral 6. Labetelol: [Combined b -adrenergic (b1 & b2) and a-adrenergic blocker] Dose : 0.2-1.0 mg/kg can be given as an IV bolus every 10 min; Dosages of 0.25 - 3 mg / kg / hr by IV infusion.. 7. Hydralazine: [Direct arterial vasodilator with no effect on venous circulation] Dose : 0.1 - 0.2 mg / kg every 2 hrs (max 10 µg / kg / min)
- 36. Indications for Renal Biopsy 1 Features of systemic illness: features. o Fever, rash, joint pain, heart disease 2Severe renal failure requiring dialysis 3 Mixed features of glomerulonephritis & nephrotic syndrome 4 Absence of serologic evidence of streptococcal infection; 5 Normal levels of C3 in the acute stage of illness 6 Severe Hypertension 7Unresolving Acute GN:- Massive proteinuria persisting > 4 wks Abnormal renal function (azotemia) - past 2 wks hematuria past 3 wks Urinary sedimentation abnormality persists >18 mo.
- 37. Post Streptococcal Glomerulonephritis Prognosis • Complete recovery in 95% cases • Complement returns to normal within 3 wks • Microscopic hematuria persists for 1-2 wks • Hypertension returns to normal in 2-3 wks • 1-5 % Mortality • 1 – 5 % develop into Chronic GN, Chronic Renal Failure
- 38. conclusion The glomerulus is the part of nephron responsible for filtration. Inflammation in glomeruli is known as glomerulonephritis. Symptoms include protein and blood in urine, edema, electrolyte imbalance, lethargy, and frothy urine. Causes of glomerulonephritis include infection, autoimmune disease, and exposure to certain medications and toxins. Diagnosis is done through urine tests, blood tests, imaging techniques, and kidney biopsy. Treatment is aimed at managing the underlying cause and preventing the progression of the disease.