1. Acute Tubular Necrosis &
SIADH By
Dr. Imran Aslam
AP North Surgical ward
MHL.

2. Acute Tubular Necrosis

4. Background Definition:
An abrupt or rapid decline in the renal function.
A rise in serum BUN or creatinine concentration, with or without decrease in urine output,
Transient and completely reversible.
Normal Urine Out Put 70ml/kg /hr

5. The most common cause of ARF in the renal category.
causes
Prerenal
Renal
Postrenal
The most common cause of ARF in the renal category.
2nd most common cause of ARF in hospitalized patients, after prerenal azotemia.
Has well defined sequence of events

6. Pathophysiology
Initiation phase characterized by acute decrease in GFR with a sudden increase in serum Cr and BUN concentrations.
Maintenance phase sustained severe reduction in GFR and the BUN and Cr continue to rise.
Recovery phase, tubular function is restored, an increase in urine volume (if oliguria was present) and gradual decrease in Cr and BUN

7. Ischemic ATN Continuum of prerenal azotemia.
Initiation phase: Hypoperfusio
n initiates cell injury that often leads to cell death.
Maintenance phase Lasts 1-2 weeks. Tubulo-glomerular
feedback also plays a role by causing constriction of afferent
arterioles by the macula densa cells, which detect and increase
salt load in the distal tubules.
Recovery phase, regeneration of tubular epithelial cells

8. Nephrotoxic ATN Shared pathophysiological features
Various mechanisms include direct toxicity, intrarenal vasoconstriction, and intratubular obstruction.

9. Ischemic ATN Subtle necrosis

10. Nephrotoxic ATN Necrosis limited to sensitive areas

11. History A good history is very important in diagnosis of ATN.
Find out about:
Recent hypotension
Sepsis
Muscle necrosis (e.g. h/o seizure, cocaine use)
Exposure to contrast or nephrotoxic medications
Hypovolumia
Other risk factors for development of ATN like underlying renal disease from DM, HTN, etc.

12. sepsis

13. Muscle necrosis

14. Causes of Ischemic ATN Systemic vasodilation – sepsis, anaphylaxis DIC
Renal vasoconstriction – cyclosporine, norepinephrine, epinephrine, amphotericin B, etc
Hyperviscosity syndrome

15. Causes of Toxic ATN Exogenous Aminoglycosides Amphotericin B
Radiocontrast media
Endogenous
Myoglobinuria
Hemoglobinuria
Crystals
Multiple Myeloma

16. Endogenous toxins

18. Workup Lab studies Serum chemistries: BUN and serum Cr concentrations
CBC
Urinalysis
Ultrasound
CT Scan
MRI
Renal USG

19. Treatment General treatment Prevention Avoid nephrotoxic agents
Dialysis

20. Prognosis
Patients with oliguric ATN have a worse prognosis than patients with nonoliguric ATN.
Rapid increase in serum creatinine (i.e. >3 mg/dL).
Of the survivors of ATN, approximately 50% will undergo into chronic state.

21. Syndrome of Inappropriate antidiuretic Hormone
(SIADH)
Syndrome of Inappropriate antidiuretic Hormone

24. Characteristics SIADH is characterized by: fluid retention
serum hypo-osmolarity
dilutional hyponatraemia
hypochloremia
concentrated urine in the presence of normal or increased intravascular volume
normal renal function

25. Pathophysiology
Inappropriate ADH secretion occurs when there is disregulation of cells secreting vasopressin in posterior pituitary
Ectopic source- ADH-secreting tum0rs

28. Causes: Increased hypothalamic production Infections
Meningitis, encephalitis, abscess, HIV
Vascular
subarachnoid or subdural hemorrhage
Neoplasm
Drugs
Chemotherapeutic agents
Pulmonary diseases
Pneumonia , Tuberculosis, Acute respiratory failure ,Positive pressure ventilation, Asthma & Atelectasis
Idiopathic

30. Signs & Symptoms Decreased / Low urine output
Symptoms of hyponatraemia
Lethargy, apathy, disorientation, muscle cramps, anorexia, agitation
Symptoms of water toxicity
nausea, vomiting, personality changes, confusion
If Na < 110 mEq/L
seizures, bulbar palsies, hypothermia, stupor, coma

31. Lethargy
vomiting

32. Seizures
Coma

33. Investigation Serum Na < 135 Serum osmolality low
Urine Na is inappropriately high, >20 mmol/L
Urine osmolality is inappropriately high,
CVP is high
CXR
CT-Scan

34. Management Demeclocycline & Lithium
Treatment of underlying medical condition if exists
Normalize serum sodium over hours
Warning, if increase Na is too fast, there is a risk for pontine myelinolysis
Normalize serum osmolality
Correct excess extravascular fluid volume
Restrict fluids
3% NaCl
Loop diuretics
Demeclocycline & Lithium

35. Management Demeclocycline & lithium Both drugs are nephrotoxic
Demeclocycline can cause nausea, vomiting, and photosensitivity
Lithium has a variety of neuropsychiatric side effects
In severe cases, haemodialysis could be used