Acute renal failure is increasingly common, particularly in elderly people, although reported incidences vary according to the definition used and the population studied. In 1993 a community based study found an incidence of severe acute renal failure (serum creatinine > 500 µmol/l) of 172 per million adults per year, of whom 72% were over 70. Age related incidence rose from 17 per million per year in adults under 50 to 949 per million per year in the 80-89 age group. More recent prospective studies report an overall incidence of acute renal failure of almost 500 per million per year and an incidence of acute renal failure needing dialysis of more than 200 per million per year. This is double the UK incidence of end stage renal disease needing dialysis5 and places high demands on healthcare resources.
Acute renal failure accounts for 1% of hospital admissions and complicates more than 7% of inpatient episodes, mostly in patients with underlying chronic kidney disease. When the condition is severe enough to need dialysis in-hospital mortality is around 50%, and it may exceed 75% in the context of sepsis or in critically ill patients
Friday, May 1, 2009
Symptoms Sorry for Lateness
Acute renal failure often does not cause symptoms that you notice. If you are already in the hospital, tests done for other problems may also detect your kidney failure. When symptoms do appear, they may include:
• Swelling, especially of the legs and feet.
• Little or no urine output.
• Thirst and a dry mouth.
• Rapid heart rate.
• Feeling dizzy when you stand up.
• Loss of appetite, nausea, and vomiting.
• Feeling confused, anxious and restless, or sleepy.
• Pain on one side of the back, just below the rib cage and above the waist (flank pain).
The symptoms can help your doctor find out what type of kidney failure is present.
• Severe dehydration, a common cause of prerenal acute renal failure, may cause extreme thirst, lightheadedness or faintness, and a weak, rapid pulse.
• A blockage in the urinary tract, which causes postrenal acute renal failure, may cause pain in the side or lower back, blood in the urine (hematuria), or reduced urine output (oliguria).
Uremic syndrome (uremia) is a serious complication of severe or prolonged acute renal failure. It can cause severe nausea, confusion, seizures, irregular heart rhythm, and fluid in the lungs (pulmonary edema).
Lungs
• Swelling, especially of the legs and feet.
• Little or no urine output.
• Thirst and a dry mouth.
• Rapid heart rate.
• Feeling dizzy when you stand up.
• Loss of appetite, nausea, and vomiting.
• Feeling confused, anxious and restless, or sleepy.
• Pain on one side of the back, just below the rib cage and above the waist (flank pain).
The symptoms can help your doctor find out what type of kidney failure is present.
• Severe dehydration, a common cause of prerenal acute renal failure, may cause extreme thirst, lightheadedness or faintness, and a weak, rapid pulse.
• A blockage in the urinary tract, which causes postrenal acute renal failure, may cause pain in the side or lower back, blood in the urine (hematuria), or reduced urine output (oliguria).
Uremic syndrome (uremia) is a serious complication of severe or prolonged acute renal failure. It can cause severe nausea, confusion, seizures, irregular heart rhythm, and fluid in the lungs (pulmonary edema).
Lungs
Spleen
About the size of a cupped hand. Intraperitoneal, in the left upper quadrant.
Largest lymphoid organ – lymphoid organs consist of the thymus, lymph nodes, spleen and are part of the immune system.
Anatomy
Relations – Posteriorly: left diaphragm, left lung, ribs 9-11. Anteriorly: stomach. Inferiorly: splenic flexure of colon. Medially: left kidney.
Structure – Entirely surrounded by peritoneum except hilum, where splenic branches of splenic artery and vein enter and leave. Lymphoid follicles found in white pulp, which is scattered in the red pulp that constitutes most of its substance. White pulp – lymphocytes form lymphoid follicles which are visible to the naked eye as whitish nodules.
Physiology
Act as specific blood reservoirs to contribute up to 100ml of blood. This is done in 2 places: venous sinuses and red pulp. Venous sinuses: act just like any other venous sinus to store whole blood. Red pulp: capillaries are permeable to red blood cells which ooze out into trabeculae, in which they are trapped – reservoir of concentrated red blood cells. Sympathetic nervous system activation causes spleen to contract and may raise haematocrit 1 to 2 percent.
White pulp – lymphoid cells manufactured, similar to lymph nodes.
As red blood cells are filtered out into the trabeculae in red pulp, the fragile ones rupture due to trauma and haemoglobin and cell stroma are digested by reticuloendothelial cells to be reused as nutrients for making new blood cells.
Reticuloendothelial cells – phagocytic cells part of cleaning system for blood, acting in concert with similar cells in venous sinuses of liver. Remove debris, bacteria, parasites etc.
Pathology
Congenital polysplenia, asplenia. Associated with other malformations, especially of cardiovascular system.
Splenomegaly – often with chronic infection. Spleen enlarges same way as lymph nodes. Cleansing function increased. May also be due to congestion caused by raised splenic venous blood pressure, neoplasms (eg. lymphoma, leukaemia), immune and storage disorders.
Infarction – pale infarcts. Due to emboli, thrombosis (eg. with sickle cell disease).
Rupture – often due to blunt abdominal trauma (eg. automobile accidents). Massive intraperitoneal haemorrhage. Emergency splenectomy.
Atrophy – due to multiple infarcts, intestinal malabsorption states (eg. coeliac disease).
Surgery
Spenectomy – removal of spleen.
Subtotal (partial) splenectomy – removal of one or more segments.
Often performed to prevent patient from bleeding to death. Does not usually produce serious side effects, especially in adults because most of its functions assumed by other reticuloendothelial organs (eg. liver, bone marrow). Greater susceptibility to infections.
Thursday, April 30, 2009
Investigation
Serum creatinine & urea
Production of creatinine principally comes from metabolism of skeletal muscles. Since the level varies a little throughout the day, 24-hour urine collection is needed to reduce errors. The variations are due to changes in hydration or posture, tubular creatinine secretion etc. It is freely filtered by glomerulus, not metabolised, little or none is reabsorbed while small amount is secreted. These properties mean the amount of creatinine filtered almost equals to that excreted. Also, it is important to note that creatinine level is related to age, sex and muscle mass. Normal range is between 0.8-1.5mg/dL (70-135μmol/L).
Urine creatinine level is also taken to calculate glomerulus filtration rate (GFR):
U x V/P where U = urine concentration of creatinine; V = urine flow (mL/min); P = plasma concentration of creatinine. Normal rages are 90-140 and 80-125 mL/min for men and women respectively.
Renal failure results in reduced excretion of nitrogenous waste, e.g. urea, in which the serum concentration would be raised. Normal range lies between 2.5 - 7.5 mmol/L.
In renal diseases, a reduced renal blood flow, damage to or loss of glomeruli, or obstructed ultrafiltration along the tubules reduce GFR. Creatinine and urea are retained and give a raised serum level. However, both serum urea and creatinine do not rise above the normal range until there is a reduction of 50-60% in GFR.
Serum potassium
One of the functions of kidney is the body regulation of electrolytes e.g potassium. When kidney function is impaired, there is a reduced reabsorption of potassium, thus increases serum potassium concentration. Hyperkalaemia particularly increases the risk of cardiac dysrhythmia. Normal level is about 190mg/L.
Renal ultrasound
This can be used to differentiate between chronic and acute renal failure, in which the former usually results in a smaller kidney. Likewise, the images confirm the presence of any bladder outflow obstruction, urethral or ureteric stricture or obstruction etc. – suggesting post-renal cause of renal failure.
Production of creatinine principally comes from metabolism of skeletal muscles. Since the level varies a little throughout the day, 24-hour urine collection is needed to reduce errors. The variations are due to changes in hydration or posture, tubular creatinine secretion etc. It is freely filtered by glomerulus, not metabolised, little or none is reabsorbed while small amount is secreted. These properties mean the amount of creatinine filtered almost equals to that excreted. Also, it is important to note that creatinine level is related to age, sex and muscle mass. Normal range is between 0.8-1.5mg/dL (70-135μmol/L).
Urine creatinine level is also taken to calculate glomerulus filtration rate (GFR):
U x V/P where U = urine concentration of creatinine; V = urine flow (mL/min); P = plasma concentration of creatinine. Normal rages are 90-140 and 80-125 mL/min for men and women respectively.
Renal failure results in reduced excretion of nitrogenous waste, e.g. urea, in which the serum concentration would be raised. Normal range lies between 2.5 - 7.5 mmol/L.
In renal diseases, a reduced renal blood flow, damage to or loss of glomeruli, or obstructed ultrafiltration along the tubules reduce GFR. Creatinine and urea are retained and give a raised serum level. However, both serum urea and creatinine do not rise above the normal range until there is a reduction of 50-60% in GFR.
Serum potassium
One of the functions of kidney is the body regulation of electrolytes e.g potassium. When kidney function is impaired, there is a reduced reabsorption of potassium, thus increases serum potassium concentration. Hyperkalaemia particularly increases the risk of cardiac dysrhythmia. Normal level is about 190mg/L.
Renal ultrasound
This can be used to differentiate between chronic and acute renal failure, in which the former usually results in a smaller kidney. Likewise, the images confirm the presence of any bladder outflow obstruction, urethral or ureteric stricture or obstruction etc. – suggesting post-renal cause of renal failure.
Prognosis of acute renal failure
For specific information, visit http://www.kidneyatlas.org/book1/adk1_08.pdf, it's an extract of a textbook and it's just AMAZING! all these pretty tables that make sense (at least most of the time), and quite detailed info. Strongly recommended. (second half of the chapter is most applicable)
Anyway, basically acute kidney failure is quite a bad thing to have, and the prognosis is very reliant on the underlying cause of the kidney failure. Despite innovations in kidney treatment, mortality from ARF have actually increased, but this can be explained away by ageing populations, more diabetics, better treatments for other causes, but then again iatropic caused ACR have also increased. Mortality is approximately 50% in population studies, but on an individual level it varies greatly.
Some of the most important variables in determining prognosis are listed here:
Age
Jaundice
Sepsis
Burns
Trauma
NSAIDs
BUN increments
Coma
Oliguria
Obstetric origin
Malignancies
Cardiovascular disease
X-ray contrast agents
Acidosis
Hypotension
Catabolism
Hemolysis
Hepatic disease
Kind of surgery
Hyperkalemia
Need for dialysis
Assisted respiration
Site of war injuries
Disseminated intravascular coagulopathy
Pancreatitis
Antibiotics
Timing of treatment
After 30 days, 90% of people who are going to recover have recovered, or who are going to die, have died, so the longer they hang in there, the better their changes are.
Seriously. just read the chapter. it's really good :)
Anyway, basically acute kidney failure is quite a bad thing to have, and the prognosis is very reliant on the underlying cause of the kidney failure. Despite innovations in kidney treatment, mortality from ARF have actually increased, but this can be explained away by ageing populations, more diabetics, better treatments for other causes, but then again iatropic caused ACR have also increased. Mortality is approximately 50% in population studies, but on an individual level it varies greatly.
Some of the most important variables in determining prognosis are listed here:
Age
Jaundice
Sepsis
Burns
Trauma
NSAIDs
BUN increments
Coma
Oliguria
Obstetric origin
Malignancies
Cardiovascular disease
X-ray contrast agents
Acidosis
Hypotension
Catabolism
Hemolysis
Hepatic disease
Kind of surgery
Hyperkalemia
Need for dialysis
Assisted respiration
Site of war injuries
Disseminated intravascular coagulopathy
Pancreatitis
Antibiotics
Timing of treatment
After 30 days, 90% of people who are going to recover have recovered, or who are going to die, have died, so the longer they hang in there, the better their changes are.
Seriously. just read the chapter. it's really good :)
Definition - Acute Renal Failure
Acute renal failure (ARF) Definition,:
Pre-renal uraemia (impaired perfusion of kidneys with blood)
Intrinsic uraemia (damage to the kidney itself)
Post-renal uraemia (obstruction in urinary tract from calyces to ext, urethral tract.)
- Abrupt deterioration in parenchymal kidney function, usually reversible. Clinically, damage should be enough to cause uraemia.
- Oliguria (dec. urine ouput) a feature usually.
- Can be life-threatening medical emergency due to drastic electrolyte imbalances.
- Acute vs chronic not readily apparent with pt. w/ uraemia. Note: acute-on-chronic cases exist
| | | | | | | | Acute Renal Failure | | | | | | |||||||||||||||||||||
| | | | | | | | | | | | | | | | | | | | |||||||||||||||
| | | | | | | | | | | | | | |||||||||||||||||||||
| | | | Pre-renal | | | Intrinsic | | | Post-renal | ||||||||||||||||||||||||
Pre-renal uraemia (impaired perfusion of kidneys with blood)
- hypovolaemia, hypotension, impaired cardiac pump efficiency, vascular disease limiting renal blood flow, combinations.
- usually can be autoregulated and GFR can be relatively maintained, progression leads to pre-renal uraemia.
Intrinsic uraemia (damage to the kidney itself)
- toxins/meds, rhabdomyolosis (breakdown of myocytes releases myoglobin which affects the kidney - can be caused by injury [especially crush or extensive blunt trauma]), haemolysis - resultant haemoglobin damages tubules, multiple myeloma, acute glomerulonephritis
Post-renal uraemia (obstruction in urinary tract from calyces to ext, urethral tract.)
- medication interfering with normal bladder emptying (e.g. anticholinergics).
- benign prostatic hypertrophy or prostate cancer.
- kidney stones.
- due to abdominal malignancy (e.g. ovarian cancer, colorectal cancer).
- obstructed urinary catheter.
- drugs that can cause crystalluria and drugs that can lead to myoglobinuria & cystitis
Acute Renal Failure- Treatment
Acute Renal Failure
Treatment Overview
The goals of treatment for acute renal failure are to:
Correct or treat the cause of kidney failure.
Support the kidneys until they have healed and can work properly.
Prevent or treat any complications caused by acute renal failure.
Treating the cause
Because treatment for acute renal failure (ARF) depends on what caused it, treatment can vary widely. Your doctor may need to:
Replace lost fluids, such as water, blood, and plasma, and restore blood flow to the kidneys. In cases of prerenal ARF caused by dehydration or blood loss, for example, kidney function may quickly return to normal after fluid and blood levels are corrected.
Discontinue any medications that may be causing the problem. These may include some antibiotics, common pain medicines (nonsteroidal anti-inflammatory drugs) such as aspirin or ibuprofen, blood pressure medicines, and medicines used to treat cancer (chemotherapy).
Treat kidney disease that is causing damage to the kidneys (intrinsic ARF) by using plasma exchange, glucocorticoids (such as cortisol), or other medicines, depending on the specific disease.
Use medicines to stop the immune system from working (immunosuppressants), such as cyclophosphamide, when an autoimmune disorder is causing acute renal failure. These disorders include lupus and other diseases that cause inflammation of the blood vessels (vasculitis).
Remove or bypass a blockage in the urinary tract (postrenal ARF). Kidney function often rapidly returns to normal after a blockage is removed and urine can flow out of the kidneys. Some blockages, such as kidney stones, can be removed. If the blockage cannot be removed, urine flow may be rerouted around the blockage using a catheter or another method. If the bladder is not emptying properly, placing a catheter in the bladder to empty it can quickly relieve symptoms and allow kidney function to return to normal.
Supporting your kidneys
Supporting your kidneys when you have acute renal failure can be complicated. Most people who develop acute renal failure are already in a hospital being treated for another medical problem and already may be critically ill before acute renal failure develops. Treating the primary medical problem may make acute renal failure worse.
As fluid and waste build up in the blood, acute renal failure can lead to severe, life-threatening complications, such as uremic syndrome (uremia) and infection (sepsis). It is important to control early complications, such as fluid overload, chemical imbalances, and anemia, so that more serious complications are less likely to develop.
Support for your kidneys so they can heal will include close management of:
Fluid intake. Fluids lost because of dehydration or blood loss must be restored, but fluid intake might also be limited, to avoid fluid buildup.
Nutrition. A specialized diet with restricted fluid intake may be used to meet nutritional needs without putting too much stress on failing kidneys.
Medications. Several medications are used to help relieve the fluid buildup that can occur in acute renal failure. Your doctor may adjust the dose of your medicines so that they work well for you. Many doctors use diuretics to improve urine output and remove excess water from the body. But some experts feel that they may not be helpful and may actually be harmful to people who are very ill.2 Depending on the cause and severity of your acute renal failure, your doctor may choose another method to get rid of extra fluids.
Causes of urinary blockage, if a blockage is present. If the blockage cannot be removed, urine flow may be rerouted around the blockage using a catheter or a small, flexible tube called a stent.
Treatment Overview
The goals of treatment for acute renal failure are to:
Correct or treat the cause of kidney failure.
Support the kidneys until they have healed and can work properly.
Prevent or treat any complications caused by acute renal failure.
Treating the cause
Because treatment for acute renal failure (ARF) depends on what caused it, treatment can vary widely. Your doctor may need to:
Replace lost fluids, such as water, blood, and plasma, and restore blood flow to the kidneys. In cases of prerenal ARF caused by dehydration or blood loss, for example, kidney function may quickly return to normal after fluid and blood levels are corrected.
Discontinue any medications that may be causing the problem. These may include some antibiotics, common pain medicines (nonsteroidal anti-inflammatory drugs) such as aspirin or ibuprofen, blood pressure medicines, and medicines used to treat cancer (chemotherapy).
Treat kidney disease that is causing damage to the kidneys (intrinsic ARF) by using plasma exchange, glucocorticoids (such as cortisol), or other medicines, depending on the specific disease.
Use medicines to stop the immune system from working (immunosuppressants), such as cyclophosphamide, when an autoimmune disorder is causing acute renal failure. These disorders include lupus and other diseases that cause inflammation of the blood vessels (vasculitis).
Remove or bypass a blockage in the urinary tract (postrenal ARF). Kidney function often rapidly returns to normal after a blockage is removed and urine can flow out of the kidneys. Some blockages, such as kidney stones, can be removed. If the blockage cannot be removed, urine flow may be rerouted around the blockage using a catheter or another method. If the bladder is not emptying properly, placing a catheter in the bladder to empty it can quickly relieve symptoms and allow kidney function to return to normal.
Supporting your kidneys
Supporting your kidneys when you have acute renal failure can be complicated. Most people who develop acute renal failure are already in a hospital being treated for another medical problem and already may be critically ill before acute renal failure develops. Treating the primary medical problem may make acute renal failure worse.
As fluid and waste build up in the blood, acute renal failure can lead to severe, life-threatening complications, such as uremic syndrome (uremia) and infection (sepsis). It is important to control early complications, such as fluid overload, chemical imbalances, and anemia, so that more serious complications are less likely to develop.
Support for your kidneys so they can heal will include close management of:
Fluid intake. Fluids lost because of dehydration or blood loss must be restored, but fluid intake might also be limited, to avoid fluid buildup.
Nutrition. A specialized diet with restricted fluid intake may be used to meet nutritional needs without putting too much stress on failing kidneys.
Medications. Several medications are used to help relieve the fluid buildup that can occur in acute renal failure. Your doctor may adjust the dose of your medicines so that they work well for you. Many doctors use diuretics to improve urine output and remove excess water from the body. But some experts feel that they may not be helpful and may actually be harmful to people who are very ill.2 Depending on the cause and severity of your acute renal failure, your doctor may choose another method to get rid of extra fluids.
Causes of urinary blockage, if a blockage is present. If the blockage cannot be removed, urine flow may be rerouted around the blockage using a catheter or a small, flexible tube called a stent.
GLOMERULAR FILTRATION
GLOMERULAR FILTRATION
- The Filtration Membrane
1. Fenestrated Endothelium (70-90nm)
- highly permeable
2. Basement Membrane (8nm)
- consists of proteoglycan gel
- blood albumin 7nm however it is negatively charged and thus repelled by the membrane
3. Filtration Slits
- located between the pedicels
- around 30nm wide
· Thus, any molecule smaller than 3nm can pass freely through the filtration membrane into the capsular space
à Water, electrolytes, glucose, fatty acids, nitrogenous wastes and vitamins
· Concentration in the glomerular filtrate is similar to that in the blood plasma
- Filtration Pressure
· BHP Blood Hydrostatic Pressure = 60mmHg
à afferent arteriole is substantially larger than the efferent arteriole
à glomerulus has a large inlet and small outlet
· CP Hydrostatic Pressure (capsular space) = 18mmHg
à (slightly negative interstitial pressures elsewhere)
à due to high filtration rate occurring in capsular space and continual accumulation of fluid in the capsule
· COP Colloid Osmotic Pressure = 32mmHg
à Similar to everywhere else
· The glomerular filtrate is almost protein-free and has no significant COP
(this can change markedly in kidney diseases that allow protein to filter into the capsular space)
THUS
o 1 high outward pressure
o 2 lower inward pressures
NFP = 60out – 18in -32in = 10mm Hg out
GLOMERULAR FILTRATION RATE
GFR = NFP x Kf = 10 x 12.5 = 125mL/min
RENAL AUTOREGULATION
- ability of the nephrons to adjust their own blood flow and GFR without external (hormonal or neuronal) control
- Two mechanisms
The Myogenic Mechanism
Tubuloglomerular Feedback
- The Filtration Membrane
1. Fenestrated Endothelium (70-90nm)
- highly permeable
2. Basement Membrane (8nm)
- consists of proteoglycan gel
- blood albumin 7nm however it is negatively charged and thus repelled by the membrane
3. Filtration Slits
- located between the pedicels
- around 30nm wide
· Thus, any molecule smaller than 3nm can pass freely through the filtration membrane into the capsular space
à Water, electrolytes, glucose, fatty acids, nitrogenous wastes and vitamins
· Concentration in the glomerular filtrate is similar to that in the blood plasma
- Filtration Pressure
· BHP Blood Hydrostatic Pressure = 60mmHg
à afferent arteriole is substantially larger than the efferent arteriole
à glomerulus has a large inlet and small outlet
· CP Hydrostatic Pressure (capsular space) = 18mmHg
à (slightly negative interstitial pressures elsewhere)
à due to high filtration rate occurring in capsular space and continual accumulation of fluid in the capsule
· COP Colloid Osmotic Pressure = 32mmHg
à Similar to everywhere else
· The glomerular filtrate is almost protein-free and has no significant COP
(this can change markedly in kidney diseases that allow protein to filter into the capsular space)
THUS
o 1 high outward pressure
o 2 lower inward pressures
NFP = 60out – 18in -32in = 10mm Hg out
GLOMERULAR FILTRATION RATE
GFR = NFP x Kf = 10 x 12.5 = 125mL/min
RENAL AUTOREGULATION
- ability of the nephrons to adjust their own blood flow and GFR without external (hormonal or neuronal) control
- Two mechanisms
The Myogenic Mechanism
Tubuloglomerular Feedback
Acute management of Trauma - Sarah
Management of Trauma
• Preparation
o Plan, team, equipment, warning
• Triage – MIST
o Mechanism – much stronger factor in paediatrics then in adults.
o Injury
o Signs and symptoms
o Treatment
• Primary survey (ABCDE)
• Resuscitation
• Secondary survey (head to toe)
• Monitoring and re-evaluation
o Urine output, kidney function
• Definitive care
o –Comprehensive management, fracture stabilisation, any operative intervention, transfer to an appropriate facility
• Tertiary survey
o –Identify injuries not initially apparent
o –Treat other conditions
ABCD – the expanded version
• A - Airway maintenance with cervical spine control
o –Cervical spine immobilisation
o –Protect the airway (clear mouth/nose, jaw thrust, Guedel airway)
o –Check trachea
• Administer oxygen
• B – Breathing and ventilation
o Symmetry, flail chest, spontaneous ventilation, air entry, breath sounds
• C- Circulation with haemorrhage control
o –Perfusion, Pulse & BP
o –IV access
o –Resuscitate
o Put in urinary catheter – measure urinary output
• D – Neurological disability
o –A Alert
o –V Voice
o –P Pain
o –U Unresponsive
o –GCS (score E+V+M=3-15)
o Observe over time – intracranial head injury
• E – Exposure, completely undress but prevent hypothermia.
o –Environmental control
o –Active warming required;
o –space blankets maintain temperature DO NOT warm the patient
Communicate and Handover (ISBAR)
• I – Identification/introduction
• S – Situation
• B – background
o e.g. Epilepsy, diabetes; find out from wife at road side, treatment of other illnesses.
• A – assessment
• R – Recommendation/request
o What you expect to happen next in the patient
• Preparation
o Plan, team, equipment, warning
• Triage – MIST
o Mechanism – much stronger factor in paediatrics then in adults.
o Injury
o Signs and symptoms
o Treatment
• Primary survey (ABCDE)
• Resuscitation
• Secondary survey (head to toe)
• Monitoring and re-evaluation
o Urine output, kidney function
• Definitive care
o –Comprehensive management, fracture stabilisation, any operative intervention, transfer to an appropriate facility
• Tertiary survey
o –Identify injuries not initially apparent
o –Treat other conditions
ABCD – the expanded version
• A - Airway maintenance with cervical spine control
o –Cervical spine immobilisation
o –Protect the airway (clear mouth/nose, jaw thrust, Guedel airway)
o –Check trachea
• Administer oxygen
• B – Breathing and ventilation
o Symmetry, flail chest, spontaneous ventilation, air entry, breath sounds
• C- Circulation with haemorrhage control
o –Perfusion, Pulse & BP
o –IV access
o –Resuscitate
o Put in urinary catheter – measure urinary output
• D – Neurological disability
o –A Alert
o –V Voice
o –P Pain
o –U Unresponsive
o –GCS (score E+V+M=3-15)
o Observe over time – intracranial head injury
• E – Exposure, completely undress but prevent hypothermia.
o –Environmental control
o –Active warming required;
o –space blankets maintain temperature DO NOT warm the patient
Communicate and Handover (ISBAR)
• I – Identification/introduction
• S – Situation
• B – background
o e.g. Epilepsy, diabetes; find out from wife at road side, treatment of other illnesses.
• A – assessment
• R – Recommendation/request
o What you expect to happen next in the patient
Wednesday, April 29, 2009
Road death tolls & ways of prevention
Long term trend in deaths
• While there is evidence of a long term downward trend in Australian road deaths, the
number of deaths per annum has not changed markedly since 2003.
Change in deaths since 2006
• In 2007, there were 1,616 persons killed in 1,466 road crashes. Compared with 2006, this was a 1.1 per cent increase in deaths and a 0.9 per cent increase in fatal crashes.
• The pattern of change varied substantially between jurisdictions.
Fatality numbers:
– Decreased in Tasmania (14.5 per cent), NSW (9.9 per cent) and Victoria (0.9 per cent).
– Increased in the Northern Territory (33.3 per cent), Western Australia (15.8 per cent),
the ACT (7.7 per cent), Queensland (7.2 per cent) and South Australia (6.0 per cent).
• Among different road user groups :
– Driver deaths increased by 4.9 per cent.
– Passenger deaths increased 1.5 per cent.
– Pedestrian deaths decreased 11.5 per cent.
– Motorcyclist deaths stayed constant.
– Cyclist deaths increased by two deaths.
Five year trends
• Between 2002 and 2007, road deaths decreased by an average annual rate of 0.9 per cent.
The average annual decrease for females was 2.5 per cent, and for males 0.3 per cent.
• Estimated five year trends varied across jurisdictions:
– The largest average annual decrease was in South Australia (5.3 per cent), followed by
NSW (3.9 per cent), Victoria (2.2 per cent) and the Northern Territory (0.4 per cent).
– The largest average annual increase was in the ACT (9.7 per cent), followed by
Tasmania (5.7 per cent), Western Australia (4.8 per cent) and Queensland (2.4 per
cent).
• Five year trends also varied across road user groups:
– Passenger deaths decreased by an annual average rate of 5.1 per cent.
– Pedestrian deaths decreased by an annual average rate of 3.1 per cent.
– Driver deaths increased by an annual average of rate 0.4 per cent.
– Motorcyclist deaths increased by an annual average rate of 3.6 per cent.
– Cyclist deaths increased by an annual average rate of 6.2 per cent.
Rates of road deaths per population
• The rate of road crash deaths per population during 2007 was 7.7 deaths per 100,000 population. This is the same as the rate during 2006.
PREVENTION
1)The Lancet medical journal on June 20, Robert Tibshirani of the Stanford University School of Medicine reported on a study of drivers in Ontario, Canada which indicated that tickets do reduce crashes and save lives. Tibshirani's research indicated that one life is saved for every 80,000 tickets, and one emergency department visit for every 1,300 tickets.
2)New technology- Intelligent Speed Adaptations (ISA) - accelerator pedals become tougher after particular speed causing you to reduce speed because its more effort.
3) The wipe off 5- the speeding campaigns
4) NO drink driving
5) Dont drive wen ure tired- the billboards with the messages to take a 15 min power nap
6) Seat belt regulations
7) What Froetscher and the National Safety Council is calling from an across the board ban on the use of cell phones while driving as studies that have been done by the government and universities have shown that hands free wireless devices have not aided in helping drivers to concentrate and might even be more dangerous in some cases.
8) Dont drive if you dont have a licence.... - Chris Brown got away with it coz he was rich ;p ...
9) Try to do one thing at a time and concentrate whilst you drive because not only are you putting your life at risk but also everyone else on the road.
References:
http://www.infrastructure.gov.au/roads/safety/publications/2008/pdf/Ann_Stats_2007.pdf
http://www.drivers.com/article/636/
http://www.readersdigest.com.au/discovery-channel-mag/new-technologies-to-reduce-road-accidents/article91290.html
http://www.lawtech2008.org/?tag=cell-phone-accident
• While there is evidence of a long term downward trend in Australian road deaths, the
number of deaths per annum has not changed markedly since 2003.
Change in deaths since 2006
• In 2007, there were 1,616 persons killed in 1,466 road crashes. Compared with 2006, this was a 1.1 per cent increase in deaths and a 0.9 per cent increase in fatal crashes.
• The pattern of change varied substantially between jurisdictions.
Fatality numbers:
– Decreased in Tasmania (14.5 per cent), NSW (9.9 per cent) and Victoria (0.9 per cent).
– Increased in the Northern Territory (33.3 per cent), Western Australia (15.8 per cent),
the ACT (7.7 per cent), Queensland (7.2 per cent) and South Australia (6.0 per cent).
• Among different road user groups :
– Driver deaths increased by 4.9 per cent.
– Passenger deaths increased 1.5 per cent.
– Pedestrian deaths decreased 11.5 per cent.
– Motorcyclist deaths stayed constant.
– Cyclist deaths increased by two deaths.
Five year trends
• Between 2002 and 2007, road deaths decreased by an average annual rate of 0.9 per cent.
The average annual decrease for females was 2.5 per cent, and for males 0.3 per cent.
• Estimated five year trends varied across jurisdictions:
– The largest average annual decrease was in South Australia (5.3 per cent), followed by
NSW (3.9 per cent), Victoria (2.2 per cent) and the Northern Territory (0.4 per cent).
– The largest average annual increase was in the ACT (9.7 per cent), followed by
Tasmania (5.7 per cent), Western Australia (4.8 per cent) and Queensland (2.4 per
cent).
• Five year trends also varied across road user groups:
– Passenger deaths decreased by an annual average rate of 5.1 per cent.
– Pedestrian deaths decreased by an annual average rate of 3.1 per cent.
– Driver deaths increased by an annual average of rate 0.4 per cent.
– Motorcyclist deaths increased by an annual average rate of 3.6 per cent.
– Cyclist deaths increased by an annual average rate of 6.2 per cent.
Rates of road deaths per population
• The rate of road crash deaths per population during 2007 was 7.7 deaths per 100,000 population. This is the same as the rate during 2006.
PREVENTION
1)The Lancet medical journal on June 20, Robert Tibshirani of the Stanford University School of Medicine reported on a study of drivers in Ontario, Canada which indicated that tickets do reduce crashes and save lives. Tibshirani's research indicated that one life is saved for every 80,000 tickets, and one emergency department visit for every 1,300 tickets.
2)New technology- Intelligent Speed Adaptations (ISA) - accelerator pedals become tougher after particular speed causing you to reduce speed because its more effort.
3) The wipe off 5- the speeding campaigns
4) NO drink driving
5) Dont drive wen ure tired- the billboards with the messages to take a 15 min power nap
6) Seat belt regulations
7) What Froetscher and the National Safety Council is calling from an across the board ban on the use of cell phones while driving as studies that have been done by the government and universities have shown that hands free wireless devices have not aided in helping drivers to concentrate and might even be more dangerous in some cases.
8) Dont drive if you dont have a licence.... - Chris Brown got away with it coz he was rich ;p ...
9) Try to do one thing at a time and concentrate whilst you drive because not only are you putting your life at risk but also everyone else on the road.
References:
http://www.infrastructure.gov.au/roads/safety/publications/2008/pdf/Ann_Stats_2007.pdf
http://www.drivers.com/article/636/
http://www.readersdigest.com.au/discovery-channel-mag/new-technologies-to-reduce-road-accidents/article91290.html
http://www.lawtech2008.org/?tag=cell-phone-accident
Diagnosis of acute renal failure
This website was awesome and has all these easy-to-read tables on how to diagnose acute renal failure:
http://www.aafp.org/afp/20000401/2077.html
The difference between acute and chronic renal failure
- Acute renal failure is a deterioration in kidney function over a period of days or weeks, which is usually reversible
- Chronic renal failure is long-standing and progressive impairment of renal function, which is usually irreversible
Three types of renal failure:
• Prerenal – diminished renal blood flow
• Intrinsic – damage to renal prenchyma
• Postrenal – urinary tract obstruction
How to diagnose:
1. Thorough history and physical examination
o Symptoms
Anorexia
Fatigue
Mental status changes
Nausea and vomiting
Pruritus (itching)
Seizures (if blood urea nitrogen level is very high)
Shortness of breath (if volume overload is present)
o Physical findings
Asterixis (flapping tremor)and myoclonus (sudden twitch of muscle)
Pericardial or pleural rub
Peripheral edema (if volume overload is present)
Pulmonary rales/crackles (if volume overload is present)
Elevated right atrial pressure (if volume overload is present)
2. Blood and urine tests
• Blood test
o BUN (blood urea nitrogen)
o Serum electrolyte
o Creatinine
o Calcium
o Phosphorus
o Albumin levels
o Complete blood count
• Urine test
o Dipstick test
o Microscopy
o Sodium
o Creatinine levels
o Urine osmolarity
3. If necessary, a renal biopsy may need to be performed if there is intrinsic renal failure that is not acute tubular necrosis.
o Complications (very low chance, less that 1%) – bleeding, arteriovenous fistula, death
Prerenal failure (problem = impaired renal blood flow – intravascular depletion, decreased effective circulating volume to kidneys or agents that impair renal blood flow):
• Urine and blood studies
o Few hyaline casts
o Urine osmolarity of greater than 500 mOsm [normal = 50-1400 mOsm/kg)
o Fraction of excreted sodium – less than 1% (kidneys respond as if volume depletion has occurred – absorb sodium to absorb water)
o Parenchyma is undamaged
Intrinsic kidney failure (injury to renal parenchyma):
• Impaired sodium reabsorption (due to parenchymal damage)
o sodium fraction excreted is greater than 3%
• Isotonic urine osmolarity – 250-300 mOsm
Postrenal acute renal failure (outflow tract of kidney/s is blocked):
• Severe oligonuria (small urine volume) or anuria
o Output less than 100 mL per day (normal = 1-2L)
http://www.aafp.org/afp/20000401/2077.html
The difference between acute and chronic renal failure
- Acute renal failure is a deterioration in kidney function over a period of days or weeks, which is usually reversible
- Chronic renal failure is long-standing and progressive impairment of renal function, which is usually irreversible
Three types of renal failure:
• Prerenal – diminished renal blood flow
• Intrinsic – damage to renal prenchyma
• Postrenal – urinary tract obstruction
How to diagnose:
1. Thorough history and physical examination
o Symptoms
Anorexia
Fatigue
Mental status changes
Nausea and vomiting
Pruritus (itching)
Seizures (if blood urea nitrogen level is very high)
Shortness of breath (if volume overload is present)
o Physical findings
Asterixis (flapping tremor)and myoclonus (sudden twitch of muscle)
Pericardial or pleural rub
Peripheral edema (if volume overload is present)
Pulmonary rales/crackles (if volume overload is present)
Elevated right atrial pressure (if volume overload is present)
2. Blood and urine tests
• Blood test
o BUN (blood urea nitrogen)
o Serum electrolyte
o Creatinine
o Calcium
o Phosphorus
o Albumin levels
o Complete blood count
• Urine test
o Dipstick test
o Microscopy
o Sodium
o Creatinine levels
o Urine osmolarity
3. If necessary, a renal biopsy may need to be performed if there is intrinsic renal failure that is not acute tubular necrosis.
o Complications (very low chance, less that 1%) – bleeding, arteriovenous fistula, death
Prerenal failure (problem = impaired renal blood flow – intravascular depletion, decreased effective circulating volume to kidneys or agents that impair renal blood flow):
• Urine and blood studies
o Few hyaline casts
o Urine osmolarity of greater than 500 mOsm [normal = 50-1400 mOsm/kg)
o Fraction of excreted sodium – less than 1% (kidneys respond as if volume depletion has occurred – absorb sodium to absorb water)
o Parenchyma is undamaged
Intrinsic kidney failure (injury to renal parenchyma):
• Impaired sodium reabsorption (due to parenchymal damage)
o sodium fraction excreted is greater than 3%
• Isotonic urine osmolarity – 250-300 mOsm
Postrenal acute renal failure (outflow tract of kidney/s is blocked):
• Severe oligonuria (small urine volume) or anuria
o Output less than 100 mL per day (normal = 1-2L)
Monday, April 27, 2009
Tasks - PCL 8
Hi Everyone
The tasks are as follows -
~ Sarah - Trauma
~ Steph - Prognosis of Acute Renal Failure
~ Lionel - Spleen
~ Dilys - Investigation
~ Ari - Treatment
~ Ambu - Symptoms
~ Jacqui - Road death and prevention
~ Rushmi - Diagnosis
~ Jemima - Measurement of Fluid Balance
~ Sam - Incidence
~ Nathan - Definition of Acute Renal Failure
~ Kylie - Function of Kidneys in fluid regulation
~ Hasif - Structures of the kidney
~ Georgia - Glomerular filtration function
Have fun!
The tasks are as follows -
~ Sarah - Trauma
~ Steph - Prognosis of Acute Renal Failure
~ Lionel - Spleen
~ Dilys - Investigation
~ Ari - Treatment
~ Ambu - Symptoms
~ Jacqui - Road death and prevention
~ Rushmi - Diagnosis
~ Jemima - Measurement of Fluid Balance
~ Sam - Incidence
~ Nathan - Definition of Acute Renal Failure
~ Kylie - Function of Kidneys in fluid regulation
~ Hasif - Structures of the kidney
~ Georgia - Glomerular filtration function
Have fun!
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