o A 70-kg patient receiving 1 g/kg per day of protein will receive 11 g nitrogen (70 g ÷ 6.25). On balance, approximately 2 g nitrogen will become nitrogenous wastes other than urea; the remaining 9 g will form urea. On the other hand, many patients with acute renal failure present with a degree of hypercatabolism. Under these conditions, urea production is greatly enhanced owing to the catabolism of endogenous proteins, and UNA can greatly exceed that predicted from exogenous protein administration alone. For example, under conditions of severe stress, endogenous protein breakdown can generate 30 g or more of urea nitrogen per day, representing the catabolism of approx-imately 200 g protein. In addition to enhanced proteolysis accompanying hypercatabolism, increased urea production is often the result of GI bleeding, with the ultimate breakdown and absorption of the blood and its proteins. There are approximately 200 g protein per liter of whole blood.
o Several studies have demonstrated that increased protein catabolism associated with stress is mediated by hormones (eg, glucagon, catecholamines, and cortisol) and cytokines (eg, interleukins, tumor necrosis factor, etc.).
o Adequate caloric intake is essential to minimize negative nitrogen balance and to improve overall survival. In the critically ill patient with acute renal failure, approximately 35 kcal/kg per day is a reasonable goal. Hyperglycemia resulting from administration of large amounts of carbohydrate can be managed with insulin. Once dialysis is initiated, replacement of water-soluble vitamins should be assured
o Renal replacement therapy can provide homeostasis of fluid, electrolyte, acid-base, and nitrogen balance. Consequently, the initiation of renal replacement therapy should be considered whenever any of these factors cannot be controlled with other therapy. At present, three types of renal replacement treatment are available for the patient with acute renal failure: intermittent hemodialysis, peritoneal dialysis, and continuous renal replacement therapy (CRRT)
o Using conventional techniques, machine-driven hemodialysis is best suited for the hemodynamically stable patient in whom solute balance is the major concern and rapid fluid removal is well tolerated. Peritoneal dialysis is preferred in the patient with significant hemorrhagic risk and in whom vascular access is difficult to obtain. Continuous hemofiltration and its related techniques are best for providing fluid removal in the patient with vascular instability or massive fluid overload. Despite these generalizations, with appropriate technical modifications, adequate renal replacement therapy can be provided by any of these methods
o Indications for Dialytic Therapy→ Fluid Overload, Electrolyte Abnormalities, Acid-Base Abnormalities, Uremia. Poorly tolerated volume overload is the most evident indication for initiating renal replacement therapy. In general, the need to relieve pulmonary vascular congestion is the most pressing issue. When hypotension is associated with edema and apparent pulmonary congestion, pulmonary artery catheter monitoring can be invaluable in determining the amount of fluid that can be removed safely. In the hemodynamically stable patient, intermittent hemodialysis can provide the most rapid removal of fluid by easily removing 1–2 L of fluid per hour by ultrafiltration. In patients presenting with massive fluid overload, continuous hemofiltration offers the best-tolerated treatment because the ultrafiltrate is isosmotic. The only renal replacement therapy capable of rapid potassium removal is machine-driven hemodialysis, providing clearance rates of 150–250 mL/min or more. Renal replacement therapies using dialysate (ie, hemodialysis, peritoneal dialysis, or continuous hemodialysis) may contain calcium concentrations of 3.5 meq/L (1.75 mmol/L of ionized calcium) in the dialysate. Therefore, successful and rapid treatment of hypercalcemia requires lower dialysate calcium concentrations of 2.5 meq/L (1.25 mmol/L) or less. Severe hypophosphatemia may complicate all renal replacement therapies, especially in patients being maintained on intravenous hyperalimentation devoid of phosphate.
o Uremic acidosis rarely generates more than 50–100 mmol acid per day and can be easily corrected by any of the renal replacement techniques. Despite associated hyperkalemia, the dialysate bath composition should include at least 2 mmol/L potassium because correction of acidosis causes a substantial lowering of serum potassium concentration. Consideration also should be given to a relatively low-calcium bath (2.5 meq/L) because overly aggressive correction of long-standing hypocalcemia may precipitate nausea, vomiting, muscle cramping, and hypertension. Lactic acid may be produced at rates of up to 50 mmol/h and usually is associated with severe hemodynamic instability. Although daily hemodialysis can provide adequate replacement of lost bicarbonate, the patient may be left with rapidly worsening acidosis during the interdialytic period. Replacement solutions containing 150 mmol/L bicarbonate can provide as much as 100 mmol/h of continuous buffer replacement, but required calcium replacement must be administered in a separate solution.
o It is reasonable to initiate renal replacement therapy when BUN is above 100 mg/dL (36 mmol/L). Nonetheless, if rapid return of renal function is anticipated (eg, in the presence of prerenal azotemia or obstructive uropathy), levels of 150 mg/dL (54 mmol/L) or more may be tolerated for a limited period. Specific indications for dialytic therapy for complications of uremia include uremic encephalopathy, pericarditis, and uremic platelet dysfunction. Slowed mentation, somnolence, and convulsions are part of the uremic syndrome and are usually associated with other neuromuscular manifestations, including asterixis, myoclonus, and muscle twitching. In general, these symptoms respond within several days after the start of dialytic therapy. Hemodialysis performed five times weekly is recommended, but means to limit anticoagulation should be employed in order to minimize the risk of hemopericardium. In patients with large pericardial effusions, early use of pericardiotomy may be recommended because aggressive hemodialysis may be associated with a high mortality rate.
o Uremic platelet dysfunction is identified most often with prolongation of the bleeding time. In general, bleeding times will normalize along with lowering of serum urea. Acutely, rapid correction of platelet dysfunction can be achieved with infusions of desmopressin at a single dose of 0.3 μg/kg.
o Many renally excreted medications require dosage modification to account for the amount removed by a given renal replacement therapy.
o In general, withholding of dialysis may be considered when there is evidence of irreversible vital organ failure or severe cerebral damage. Most forms of acute renal failure reverse within 8 weeks. If renal failure persists beyond this period, one should initiate plans for maintenance dialysis therapy.
o Hemodialysis→ Intermittent hemodialysis is the most widely used technique for acute renal failure. In general, 4-hour treatments performed three times weekly are sufficient to provide adequate replacement in the oliguric or anuric patient. Disadvantages include relatively rapid fluid removal, which may be poorly tolerated. Other disadvantages of hemodialysis involve the need for large-bore hemoaccess and anticoagulation of the extracorporeal circuit. Most modern dialyzers provide 150–250 mL/min of urea clearance with blood flows between 200 and 300 mL/min. More rapid solute clearance can be obtained with the newer more porous filters, especially when operated at blood flows of up to 400 mL/min or more. Currently available dialyzers also can produce between 1 and 3 L of ultrafiltrate per hour, usually limited by the patient’s hemodynamic stability. A rel-atively gentler type of hemodialysis involves the prolongation of the treatment in a low-efficiency mode. These slow, low-efficiency dialysis (SLED) treatments are applied from 8–18 hours at a time and allow for less aggressive fluid removal. “High flux” dialyzers provide the most rapid solute clearance, but their use requires dialysis equipment with volumetric control of fluid removal. . In the acute setting, the most widely used method is the percutaneous cannulation of either the femoral or subclavian vein with double-lumen catheters. The right internal jugular vein offers an alternative to subclavian cannulation. The need for anticoagulation can be the most significant disadvantage associated with hemodialysis. During treatment, the most commonly encountered complication is hypotension. Other complications include cardiac arrhythmias, hypoxemia, hemorrhage, air embolism, pyrogenic reactions, and dysequilibrium syndromes. first-use syndrome has been managed with intravenous aminophylline or subcutaneous epinephrine. If serious hemorrhage occurs during dialysis, previously administered heparin should be neutralized with protamine..
o Peritoneal Dialysis→Peritoneal dialysis offers the best method of renal replacement for the patient in whom it is difficult or impossible to obtain adequate hemoaccess. In contrast, patients with recent abdominal surgery may be poor candidates owing to the risks of abdominal wound dehiscence and infection of recently implanted vascular grafts. A major advantage of this technique is that no anticoagulation is required. Disadvantages include substantial protein loss risks of peritonitis, drainage difficulties, compromised pulmonary function owing to elevated diaphragms, hydrothorax, glucose and electrolyte abnormalities, and a relatively immobile patient. Solute removal with this technique depends mostly on dialysate volume and how long the dialysate is allowed to stay in the peritoneal space before drainage (dwell time). A reasonably aggressive schedule incorporates 2-L exchanges every 2 hours. A more modest schedule would be similar to that of chronic ambulatory peritoneal dialysis (CAPD), with 2-L exchanges every 4–6 hours. There are two widely used methods for obtaining access to the peritoneal cavity. Bedside placement of a stiff Teflon catheter is the most rapid means of access. Complications include bowel perforation, bladder perforation, pericatheter leakage, hemorrhage, and infection. Foley catheter placement to ensure bladder decompression prior to insertion is strongly recommended. The surgical placement of a pliable Silastic catheter (Tenckhoff type) is the safest method of obtaining access. The most common complication of peritoneal dialysis is failure to drain or insufficient drainage. If fluid infusion is obstructed, the catheter may suffer from intrinsic blockage, and an attempt at declotting may be appropriate with saline flushes or thrombolysis with urokinase or tissue plasminogen activator. Peritonitis arises most often from contamination during bag exchanges, although intraperitoneal contamination also can occur as a result of intraabdominal disease. Clinical signs of peritonitis include abdominal pain, nausea, cloudy dialysate effluent, and loss of ultrafiltration (decreased fluid output per exchange). As opposed to spontaneously occurring peritonitis, peritoneal infection in the context of peritoneal dialysis may be managed successfully with intraperitoneal antibiotics.
o continuous renal replacement therapy (CRRT )→ applied to a wide array of extracorporeal techniques. Originally proposed as a simple method of filtration powered by arteriovenous circuits and known as continuous arteriovenous hemofiltration (CAVH). Several technical modifications have been developed to enhance the efficiency of the treatment. These include the addition of a diffusive component to solute removal, known as continuous arteriovenous hemodialysis (CAVHD), and the development of specialized machines for providing continuous pumped filtration allowing for a new set of extremely efficient techniques that do not require arterial access and that no longer depend on the variability of the patient’s changing blood pressure-continuous venovenous hemofiltration (CVVH), continuous venovenous hemodialysis (CVVHD), and continuous venovenous hemodiafiltration (CVVHDF). The continuous therapies have several potential advantages over intermittent dialytic techniques. The most obvious is that the treatment is continuous, allowing for a constant readjustment of fluid and electrolyte therapy and the administration of large amounts of parenteral nutrition without the risk of interdialytic volume overload. The following techniques for continuous renal replace-ment therapy are available.
o Continuous Arteriovenous Hemofiltration (CAVH)→ The standard CAVH circuit allows blood to flow from an arterial access through a tubing circuit to a low-resistance hemofilter and back to a venous access. the popularity of CAVH has decreased, and this arteriovenous method is being replaced with blood pump-driven venovenous systems
o Slow Continuous Ultrafiltration (SCUF)→ Blood pressure-driven filtration is a means of providing continuous isoosmotic fluid removal for aid in the management of oliguric patients. The circuit is similar to that of CAVH, but no replacement fluid is administered. Although insufficient for adequate solute removal, this technique has been found useful as a means of maintaining fluid balance in patients intolerant of aggressive fluid removal and in those with cardiodynamic instability such as may be seen during aortic balloon pumping or during open-heart surgery.
o Continuous Arteriovenous Hemodialysis and Hemodiafiltration (CAVHD)→ The circuit is essentially the same as that for CAVH but with the addition of a constant infusion of dialysate passing through the filtrate compartment of the filter. The major advantage of this system is the enhanced solute clearance, which has allowed the technique to be applied to certain intoxications.
o Continuos Venovenous Hemofiltration (CVVH)→ This circuit requires a blood pump and an air detector and is often equipped with arterial and venous pressure monitors. This technique has the clear advantage of avoiding the potential complications of arterial access and is capable of providing a substantial amount of convection based clearance.
o Component to the CVVH system allows for the maximum clearance capabilities of any Continuous Venovenous Hemodialysis or Hemodiafiltration (CVVHD/F)- The addition of a diffusive of the continuous therapies.
o The blood pressure-driven treatments (ie, CAVH and CAVHD) require large-bore arterial and venous access. The most widely used is the combined cannulation of the femoral artery and vein. Hemoaccess for pump-driven continuous therapies (ie, CVVH and CVVHD) does not require arterial catheterization and uses the same access as for machine-driven hemodialysis.
o Normal fluid restriction for a patient receiving maintenance hemodialysis (three times weekly) often depends on the patient’s tolerance for aggressive fluid removal during each treatment. In general, fluid restriction should be 1–1.5 L/day and is dictated by the patient’s tendency to develop hypertension or pulmonary congestion in the interdialysis period.
o Nitrogen balance studies in hemodialysis patients suggest that protein requirements are between 1 and 1.2 g/kg per day. The caloric requirement to maintain neutral nitrogen balance is 37 kcal/kg per day. Patients receiving chronic ambulatory peritoneal dialysis lose a substantial amount of protein in the dialysate (approximately 10 g/day), and their protein requirements approach 1.4 g/kg per day.
o There are two commonly used means for creating a subcutaneous arteriovenous connec-tion: surgical anastomosis of an artery and vein, often in the wrist (primary arteriovenous fistula), and placement of a polytetrafluoroethylene graft between artery and vein in the brachial fossa. The primary arteriovenous fistula is more resistant to infection and thrombosis, but it requires up to 6 weeks to mature, and its placement is surgically impossible in many patients with inadequate distal vasculature. Polytetrafluoroethylene grafts are available for use within 1–2 weeks but are more prone to infection and pseudoa-neurysm formation.
o Chronic ambulatory peritoneal dialysis (CAPD) commonly involves four 2-L exchanges per day. Net fluid removal depends on the rate of exchange and the dialysate glucose concentration (eg, 1.5%, 2.5%, or 4.25%).
o Medical conditions requiring hospitalisation→ Medical Management of AKI, Medical Management of Nephrotic Syndrome, Medical Management of Rapidly Progressive Renal Failure, Medical Management of Chronic Renal Failure 1 (Crf ), Maintenance Hemodialysis For Crf, Medical Management of Acute Glomerulo Nephritis
o Surgical conditions & procedures requiring hospitalisation→ Renal Transplantation (A.V. Fistula surgery (creation) [Pre-Transplant Procedure Only], Renal Transplantation Surgery, Post Renal Transplant Immunosuppressive Treatment From 1st To 6th Months, Balloon dialatation of transplant Renal Artery stenosis ) CAPD-Tenchkoff catheter insertion, CAPD-Tenchkoff catheter removal, Open Pyelolithotomy, Open Nephrolithotomy, Open Cystolithotomy, Laparoscopic Pyelolithotomy, Cystolithotripsy, PCNL, Extracorporeal shockwave lithotripsy (ESWL), ursl, Nephrostomy – Lithotropsy, Dj Stent, Single Stage Urethroplasty for stricture Urethra, Stage 1 Urethroplasty for stricture Double Stage, Stage 2 Urethroplasty for stricture Double Stage, Reconstruction procedure Urethroplasty for stricture, Single Stage HYPOSPADIASIS, Stage-1 HYPOSPADIASIS, Stage-2 HYPOSPADIASIS, Transurethral resection of bladder tumour (TURBT), Post Renal Transplant Immunosuppressive Treatment From 7th To 12 Th Month., Nephrostomy – Renal, Nephrectomy for Pyonephrosis/Xgp, Simple Nephrectomy, Laproscopic Simple Nephrectomy, Laproscopic Radical Nephrectomy, Lap. Partial Nephrectomy, Bilateral Nephroureterectomy, Renal Cyst Excision, Anatrophic Peylolithotomy For Staghorn Caliculus, Endoscope Removal Of Stone In Bladder, Anderson Hynes Pyeloplasty, Excision of Ureterocele with Ureteric Implantation, Balloon dilatation of Ureteric stricture, Surgical correction of Vesicovaginal Fistula, Epispadiasis – Correction, Closure Of Urethral Fistula, Optical Urethrotomy, Perineal Urethrostomy, Ureteric Reimplantations, Surgical Procedure for Ileal Conduit Formation, Surgical corrrection of Ureterocele, Transurethral Resection of Prostate (TURP), Mid urethral sling procedure for stress urinary incontinence, Transurethral Resection of Prostate (TURP) Cyst Lithotripsy, Open Prostatectomy, Open radical Prostratectomy, Caecocystoplasty, Total Cystectomy, Partial Cystectomy, Bladder Diverticulectomy, Surgical Management of Incontinence Urine (Female), Surgical Management of Incontinence Urine (Male), Bladder neck reconstruction for Incontinence.
5’o clock: Nervous system
o Coma represents a global failure of brain function. The first responsibility of the physician caring for a patient in coma is to ensure that breathing, circulation, and nutrition are maintained. The cause of coma then must be determined and reversible causes treated appropriately.
o Normal consciousness has two main components: content and arousal. They have different anatomic substrates, with the former localized largely in the cerebral cortex and the latter depending on the brain stem reticular activating system. Injury to the dominant cortical hemisphere leads to impairment or loss of language function, but bilateral cortical injury is required for complete loss of consciousness. Furthermore, the cortex is responsible for interpreting incoming signals. This includes encoding and assigning “meaning” to emotional and sensory inputs. When the cortex is diffusely injured, the ability to reflect on and interpret experience is lost, and for this reason, the content of consciousness is lost as well
o The major role of the brain stem reticular activating system is to arouse and alert the cortex so that the organism can reflect on and react to stimuli from the environment. A patient can lose consciousness by two different mechanisms: diffuse dysfunction of the cerebral cortex or injury to the reticular activating system. Coma often develops as a result of injury to both areas. However, cortical neurons are extremely sensitive to a variety of metabolic and toxic injuries, including hypoxia, hypercapnia, hyponatremia, hypernatremia, hypoglycemia, hyperglycemia, and many drugs, whereas the brain stem is more resistant to these injuries. Thus toxic and metabolic injuries first cause dysfunction in cortical neurons, and only with increasing severity influence the brain stem. In contrast, coma owing to primary brain injury affects the reticular activating system. These major anatomic differences allow the clinician to distinguish metabolic from structural causes of coma.
o In comas owing to metabolic encephalopathy, a profound and diffuse decrease in cerebral glucose metabolism has been shown using positron-emission tomography. Similarly, severe and diffuse cerebral hypoperfusion as measured with 133Xe appears in patients in coma owing to sepsis, hepatic encephalopathy, hypoxia, head trauma, and cocaine intoxication. Studies in comatose patients using 31P magnetic resonance spectroscopy have shown dramatic decreases in the brain’s energy-containing phosphorus compounds, including ATP and phosphocreatine. This work suggests that any process that compromises cortical neuronal energy pro-duction may lead to a comatose state
o Rapidity of onset is an important clue to the cause of coma. Certain metabolic insults such as hypoxia, ischemia, or hypoglycemia may come on suddenly, whereas others such as hyponatremia, hypernatremia, and hyperglycemia develop subacutely. Similarly, subarachnoid hemorrhage or brain stem ischemic stroke can lead to sudden coma, whereas coma related to chronic subdural hematoma, cortical ischemic stroke, or brain tumor usually develops slowly.
o The five main areas that need to be assessed in the evaluation of a patient in coma are 1. level of consciousness,2. pupillary responses and ophthalmoscopic examination 3. oculomotor system,4. motor system,and 5. respiratory and circulatory systems.
o Based on the findings in these domains, usually it is possible to localize accurately the specific regions in the brain that are impaired.
o Level of Consciousness→Many terms such as stuporous, lethargic, drowsy, and semicomatose have been used to characterize degrees of altered consciousness. However, it is better to describe the patient’s spontaneous activity, response to verbal stimuli, and reaction to painful stimuli in precise terms that do not have different meanings to different observers. With herniation from a large unilateral cerebral hemisphere mass, drowsiness occurs when the reticular activating system in the thalamus is compressed; coma ensues when injury to the reticular activating system reaches the midbrain. The best places to apply painful stimuli to determine arousability are over the sternum or the nail beds; these maneuvers also help to determine whether the patient responds with evidence of focality, for example, if there is no movement of one side while the other hand attempts to remove the painful stimulus.
o Pupillary and Ophthalmoscopic Evaluation→Perhaps no component of the neurologic examination is as valuable for differentiating metabolic or toxic coma from coma owing to structural brain disease as inspection of the pupils. Pupillary size is determined by the relative contributions of the parasympathetic and sympathetic autonomic fibers. Coma associated with brain injury usually exhibits changes in the pupillary response. These changes occur because most structural comas are associated with injury to the reticular activating system in the brain stem where the Edinger-Westphal and sympathetic autonomic fibers are located
o With acute injury to the midbrain, the pupils become fixed in midposition as a result of simultaneous injury of sympathetic and parasympathetic fibers. In contrast, injury to the pons often is associated with pinpoint, minimally reactive pupils. Lateral tentorial herniation of the temporal lobe may result in compression of the third cranial nerve and the parasympathetic fibers traveling with it, causing dilation of the pupil on the side of the herniation. In some lateral herniations there will be compression of the contralateral third nerve against the edge of the tentorium.
o A major characteristic of coma owing to metabolic diseases is sparing of the pupillary response. This occurs because metabolic coma causes selective dysfunction of the cortex, whereas the centers in the brain stem that control the pupils are spared. Many comas owing to drugs spare the pupils, although some commonly used drugs do influence the pupillary response
o The ophthalmoscopic examination can provide valuable information. Papilledema usually implies increased intracranial pressure, whereas subhyaloid hemorrhage, which appears as a fresh, red flame-shaped hemorrhage between the retina and vitreous, is virtually pathognomonic of subarachnoid hemorrhage
o Despite the importance of the ophthalmoscopic evaluation, under no circumstances should the pupil be dilated in a comatose patient because changes in the pupils are often the most reliable clinical indication of deterioration following brain injury
o Oculomotor System→ As with pupillary responses, changes in the oculomotor system often occur with primary neurologic injury. The system responsible for moving the eyes is located between the sixth nerve in the pons and the third nerve in the midbrain. Closely adjacent to the sixth nerve is a gaze center known as the pontine paramedian reticular formation (PPRF). Just prior to moving one of the eyes laterally, which is accomplished with the sixth nerve, there is rapid firing in the PPRF. The contralateral eye will deviate medially via fibers that travel from the PPRF, cross in the pons, and travel medially to the contralateral third nerve nucleus in the medial longitudinal fasciculus
o The simplest way to test the viability of this system is the oculocephalic (“doll’s eye”) reflex. For this test, the patient is positioned with 30-degree neck extension, and the head is moved from side to side. If the brain stem PPRF and the vestibular system are intact, the eyes should move smoothly in the direction opposite to that in which the head is moved. A more precise test is the caloric oculovestibular response. For this test, the comatose patient is elevated to a 30-degree angle, and one tympanic membrane is irrigated with ice cold water. Ten milliliters usually is sufficient to produce a response. Within 1–2 minutes, both eyes should deviate laterally toward the side where the cold water was instilled. In metabolic or toxic coma this system is spared, whereas in many structural comas the oculovestibular system is impaired; in brain death, it is absent. In the normal, awake patient, slow deviation toward the side of the stimulus is lost, and nystagmus in the contralateral direction is observed.
o Motor Systems→Primary brain lesions often are associated with focal motor deficits, but in metabolic or toxic states, focal motor findings are normally absent. With lateral cortical or internal capsular injury, the examination shows contralateral motor deficit. Posturing in flexion (decorticate posturing) supervenes when diffuse dysfunction of the diencephalon occurs. Injury of the brain stem motor systems between the red nucleus in the midbrain and the vestibulospinal nuclei in the medulla leads to an abnormal extensor response in the arms with flaccid or extensor response in the legs (decerebrate posturing). Injury to motor systems at or below the level of the vestibulospinal nuclei results in flaccidity. With progressive neurologic injury, moving from higher to lower centers, one sees a progression from paralysis to flexor posturing to extensor posturing to flaccidity.
o Respiratory and Circulatory Changes→With injury at the level of the pons, abnormal respirations may occur. Once the medulla is injured, there is loss of respiratory function, and apnea ensues. Similarly, in the beginning stages of medullary compression, abnormalities in blood pressure, usually hypertension can present. As the medullary injury progresses, hypotension intervenes.
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