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The Miracle
INTRO.
renal failure refers to a state of sudden
RENAL FAILURE
deterioration of renal function resulting in retention of nitrogenous wastes and biochemical derangement
/kg/h) or anuria is the most prominent feature. Although urine output may be normal or only slightly reduced (non-oliguric ARF)
EG. ARF associated with nephrotoxic drugs. Increase blood level of urea and creatinine suggest the diagnosis in such case
renal disease is called Acute-ohchum renal failure. ARF comprises of 1.5 2% of all paediatric in-pt at major hospitals and 20% percent of paediatric intensive care unit
CAUSES OF ARF
CAUSES OF ARF
Pre-renal failure is renal insufficiency due to inadequate renal blood flow. Hypovolemic pre-renal failure, if treated early, responds to a fluid challenge with resumption of normal urine output and resolution of azotemia
CAUSES
CAUSES OF PRE- RENAL ARF 1) Acute gastroenteritis with dehydration and shock is a frequent cause of ARF in the part of the world 2) Burns. 3) Blood loss 4) Shock 5) Fulminant hepatitis
CAUSES
6) Congestive heart failure 7) Hepato-renal syndrome 8) Reye syndrome CUSESE OF INTRINSIC. Intrinsic Renal Disease Glomerular 1) Acute GN (APSGN) other infection 2) Cresentic GN
CAUSES OF ARF
3) Acute tubulointerstitial Nephritis 4) Acute tubular Necrosis 5) other Prolonged pre renal insult - Intravascular haemolysis( G 6PD), -Sepsis with multiorgan failure, -Nephrotoxic agent, -Snake bite, other envenomation, - P faciparum malaria, - leptospirosis
CAUSES OF ARF
CAUSES OF POST RENAL -Post-renal ARF occurs from obstruction in the urinary collecting system in the absence of renal parenchymal disease. -It is potentially reversible when the urinary tract obstruction is alleviated. -NB: Both pre and post renal condition can, if prolonged,
lead to parenchymal injury to the kidneys (intrinsic)
CAUSES Bilateral obstruction at pelvi ureteric junction, Both ureteric Obstruction, bladder outlet and urethral Obstruction by calculi, blood clots and pus debris .
INDICES FOR DIFFERENTIATING PRE-RENAL FROM INTRINSIC Pre-renal Intrinsic Urinary Na MEq/l < 20 > 40 Urinary Osmolality (mosm/kg) > 500 < 300 Blood Urea/cr. ratio > 20:1 < 20:1 Urine to plasma osmolality > 1.5 < 0.8 1.2 Fractional excretion of Na <1 >1
SIGNS
Pallor Dehydration Tachypnoea Hypotension/hypertension Mental clouding and confusion Asterixis Pericardial rub
MANAGEMENT
A)Urine Tests - Urinalysis with SG, urine m/c/s - Urine Osmolality, Na, Fractional Excretion of Na B) Blood Test - Serum e/u/cr, FBC, Blood culture, Blood gases, Peripheral Blood smear feature of micro angiopathy haemolysis, thrombocytopenia,and reticulocytosis indicate HUS. - Other test like ASO and C3 level as indicated.
(D) OTHERS
- Electricardigraphy (ECG) - Immunlogical study - Antinuclear antibody - Anti neutrophil cytoplasma antibody - Anti streptolysin o ASO titer
TX
Removal and treatment of offending agents (causes)
- History evaluation - Treatment of infection - Blood transfusion - Fluid replacement -Treatment of Hypertension - Correction of renal artery stenosis - Surgical relief of obstructive uropathy
- STOP - diuretic, NASIDS, ACE inhibition, - Inotropic for (cardiac failure) - Pressor agents, and antibody for sepsis. (2) Acute Tubular Necrosis Rx: supporting care, discontinue drugs or toxin, treat cause of circulatory failure. (3) GN Rx: supporting care if post infectious, antibody if associating with shunt infection or endocarditis, consider immune suppressive medication.
PHARMACOLOGICAL TREATMENT
(1) Diuretics- If urine output is less than 0.5ml/kg/hr in pre-renal after two hours and there is no sign of intravascular volume deficit , 2 3mg/kg of frusemide is administration. - If no urine output occur in the following hour, intrinsic renal failure is strong suspected. ( (2) Dopamine Infusion, in low dosage 1-3micg/kg/min/ cause renal vasodilation and increase renal perfusion and has been used in pt with incipient ARF, not routinely recommendation. (3) Others- - H2 blocker in stress gastritis - Anti BP drugs if HBP - Antibiotics - Heamatinics in blood loss
COMPLICATION
(1) Fluid Overload -Rx Fluid restriction (2) Pulmonary oedema /pericardial effusion Rx: Oxygen, dopamine 5 10mg/kg/min with Minimum fluid, frusemide 2 4mg/kg and monitor by CVP line, dialysis with hypertoni glucose. (3) Hypertension: symptomatic - Nitropruside, 0.5 8mg/kg/min infusion , frusemide 2-4mg/kg Asymptomatic Nifedipine 0.3 0.5mg/kg oral. Maintenance t with oral- Nifedipine, hydralizin or atenolol.
COMPLICATION
(4) Metabolic Acidosis (5) Hyper Kalaemia Acute emergency- Rx: Calcium gluconate 10% 0.51ml/kg (5 10 mins) OR Salbutamol 5 10mg nebulizer less emergency-a) NaCo3 (8.4%) 1 2ml/kg (5-20mins) (b) Glucose 50%, 0.5 1/kg with 0.1 0.2IU/kg insulin (c) Ca resonium 1g/kg/day (d) Heamodialysis (5) Hyponatremia: Fluid restriction if sensorum alteration or seizure - 3% saline 6-12m/kg over 30-90 mins
COMPLICATION CONT.
(5) Hyponatremia: Fluid restriction, if sensorial alteration or seizure Rx- 3% saline 6-12ml/kg over 30-90 mins (6) Anaemia pack red cell 10ml/kg or consider EBT (7) High serum phosphate: phosphate binders (calcium carbonate, acetate and Dietary Phosphate restriction)
(1) Ureamia Altered senserum, abnormal behavior, seizure, nausea peri- carditis. (2) Hyper Kalaemia K > 6.5 m Eq/L , K 5.5 6.5 m Eq/L with ECG change (3) Hyponatrema Na < 120 125 m Eq/L esp if symptomatic
(4) Metabolic acidosis PH < 7.2 despite NaHCO3 therapy, or NaHCO3 administration not feasible because of fluid overload. (5) Hypercatabolic state marked tissue injury, crush-syndromes, burns, sepsis, tumor lysis syndrome.
PROGNOSIS/FOLLOW
is defined as irreversible deterioration of renal function, which gradually progress to end stage renal disease ESRD.
It is characterized by a fall in
glomerular filtration rate GFR below 80mls/min/1.75m3 (100ml) for over 3 months and often accompanied by other biochemical abnormality.
per million of the population develop CRF per years. There are studies suggesting an increase in the incidence of CRF in Nigeria.
management of some cases of chronic renal disease may prevent or retard the progression of the disease into ESRF
failure and end stage renal disease denote advanced renal damage for which renal replacement is the only option
are condition that has potential to cause progressive loss of kidney function and eventually lead to CRF.
patient with kidney damage or decreased level of renal function for three months or more irrespective of the
underlying condition, and is defined as the presence of kidney damage or GRF below 2 60ml/min/1.73m
of GFR, which is estimated from the level of serum Cr and height using the Schwartz formular:
Classification of Stage
Stage GFR (ml/min/1.73m2) 90 60 89 Description
1
2.
Kidney damage with normal GFR Kidney damage with wild reduction of GFR
Classification of Stage 3. 4. 30 59 Moderate reduction of GFR 15 29 Severe reduction of GFR < 15 END STAGE (DIALYSIS)
5.
urinary infection and renal scaring Obstructive uropathy Prior history of acute Nephritis or Nephrotic syndrome Children with history of renal failure in pre natal period
cystic kidney or genetic renal condition Renal dysplasia or hypoplasia Low birth weight infant
Schonlein purpura Presence of diabetes, hypertension Systemic lupus Erythematosis and vasculitis
CAUSES OF CRF Chronic Glomerulonephropathies constitutes the most cause of CRF in childhood, especially in the older child. Chronic pyelonephritis, associated with severe urinary tract malfunction like severe vesico-uretric reflux and obstruction uropathies such as posterior urethral valves in boys are significant cause of CRF.
CAUSES OF CRF
Renal dysplasia is often suggested
by concomitant presence of other congenital abnormalities. Other renal cause of CRF include haemolytic ureamic syndrome, congenital single kidney, bilateral renal hypoplasia , bilateral wilms tumor and cystinosis.
SYSTEMIC MANIFESTATION
The clinical feature of CRF include
- itching
-hyperkalaemia, - pulmonary oedema
- altered sensorum
SYSTEMIC MANIFESTATION
The possibility of CRF should be
considered when one or more of these manifestation are present without an obvious cause. Other manifestation include, lack of energy, increase sleep, poor school performance, platelet dysfunction, and depressed cell mediated immunity, Gastric ulceration, severe itching.
In CRF there is derangement of the function of the body resulting in acid-base disturbance, disturbance of salt and wate metabolism, various metabolism bone disorder, Anaemia, central nervous system, cardiovascular, endocrine, gastrointestinal and immunological disturbances as well as disturbances of nitrogen, carbohydrate and lipid metabolism.
occur in CRF and is due primarily to reduction in the synthesis of erythropoietin by the diseased kidney. Other causes of anaemia are hymolysis due to uremia and chronic blood loss from bleeding the gastrointestinal tract, and skin and mucosa membrane as result of bleeding disorder especially abnormal platelet homeostasis
2) Gastrointestinal: Acute
gastrointestinal ulceration, peptic ulcer disease, idiopathy ascitis and petechial haemorrhage from the gut, have been described with uraemic syndrome
hormones with absence of the pubertal growth spurt, delayed menarche and puberty with absent of secondary sexual characteristics has been frequently described in CRF. There also, is low level of serum thyroxine and abnormally elevation fasting growth hormone level, which explain the glucose intolerance in uraemia.
A drop in GFR to about 20 30 ml/min/1.73 result in retention of fixed acid and a state of metabolism acidosis occur with increase in urinary excretion of calcium. There is depression of serum bicarbonate reabsorption in the proximal tubule, with a small percentage of the filtered load reabsorbed in the distal portion of the nephron. Failure to reabsorbed the filtered bicarbonate completely lead to urinary loss of this buffer and elevated urinary PH and limitation in the ability of the kidney to execute net acid and result in metabolism acido.sis
5)
Cardiovascular
-Mechanism of uraemic heart disease include fluid overload from salt and water retention, system arterial hypertension . other are anaemia, uraemia, electrolytes derangement K, Na, Ca , Mg. -Peri carditis with or without peri cardial effusion is frequently observed in patient with CRF and acute left ventricular failure and pulmonary oedema is a well known presenting feature in children with CRF -Majority of children with CRF has abnormal ECG finding and cardiovascular complication is cause of death on majority of cases
and consist of various neurological pretention. - non- specific general depression of cerebral function, fatigue, listlessness, drowsiness, poor concentration at school, to frank psychosis, hallucination, seizure and coma with decorticate posture.
-Focal neurological sign may occur but are rare; more often being associated with hypertension encephalopathy or intracranial haemorrhage. -The exact pathophysiology of this cerebral dysfunction is unknown. - The degree of dysfunction is not commensurate with level of urea and Cr in the blood probably other biochemical metabolism in the blood are responsible
manifestation of CRF in adult with restless leg syndrome, characterized by peculiar creeping, prickling and tingling sensation in the lower limb.
Often worse in the night, other
subsequent develop with loss of vibration position, touch and pain sensation and loss of deep tender reflex. In children, frank peripheral neuropathy is rare but defect in nerve condition velocity are common.
7) Immunology
Suppression of normal immune mechanical form a part of the uraemic syndrome. Various degree of lymphopenia, delayed hypersensitivity reaction, abnormal polymorphonuclear, and monocyte function as well abnormal inflammably responses have been described. 8) Renal osteodystrophy
MANAGEMENT
1)
Serum e/u/cr: Ur level is serum generally above 6mg% while serum Cr is also 100ml/L. If serum Ur is abnormally high for an elevation serum Cr due to inability to eat, estimated urea level should be calculation from the creature urinary the ratio Urea Cr 1:17
2) Serum HCO3 is often low 3)Calculation of the eGFR 4) Serum calcium may be low, normal or high
MANAGEMENT
Other Investigation CXR cardiomegaly X-ray of Hand and wrist will show the
earliest radiological changes. If present, will subperiosteal erosion of the radial aspect of the middle phalange. Total skeletal surgery is unnecessary in detecting Ros. MCU IVP
MANAGEMENT
Treatment 1) Conservative Management
-When GFR is above 10ml/min/1.73 -Occasional when patient are receiving RRT -Oliguric or anuric pt should receive fluid equal to their insensible loss plus the urine out put in 24hrs to prevent fluid overload, i.e. fluid restoration. -If serum bicarbonate is 15mm/L or less, sodium bicarbonate may be given in a dose of 1ml/kg/day
MANAGEMENT
Avoid excessive salt intake with resultant fluid
overload 1.25 dihydoxy cholecalciferol or the synthezised ,1 hydoxy cholecalciferol In dose of 10 15mg/kg/day Anti HBP, particularly blocker (if there is no cardiac failure) Hydralazin control HBP ACEI useful in renal Hypertension Phosphate binder e.g. calcium carbonate.
MANAGEMENT
Low protein diet to prevent hyperfiltration and have been used to delay the onset of end stage renal esp in adult but in children, taking into consideration the growth most children will require 2g/kg/d of high molecular value. The use of Recombinat human erythropoietin therapy has markedly diminished the need to frequent blood transfusion in children with CRF in whom often iron therapy does not correct the anaemia.
must be given to prevent impeding death. This should be done when GFR is less than 10ml/min/1.75. Dialysis- PD - HAEMODIALYSIS RENAL TRANSPLANTATION
Dialysis
Chronic Ambulatory Peritoneal Dialysis (CAPD),
which is prefer by most central and can be done in very small children aged less than 2 years in whom renal transplantation is difficulty Ad: Better growth rates less restriction diet and fluid allowance, freedom to attend activities, less requirement for blood transfusion. Other peritoneal dialysis - Continuous Cycling Peritoneal Dialysis (CCPD) - Intermittent Peritoneal
Heamodialysis
Heamodialysis: especially
Renal Transplantation
to most children and cadaver or living donor can be used. Immunosuppressive therapy such as Azathioprine, Prednisolone or cyclosporin A . For life is mandatory to prevent host grafting rejection.