Professional Documents
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General Management principles are first and foremost to relieve the obstruction. In the
case of our patient, surgical intervention was done with the installation of the
nephrostomy. Once thats taken care of, we can address the damage done to the
kidneys.
First we optimize hemodynamics with fluid resuscitation and vasopressors to keep the
kidneys well perfused. This was not done to our patient, because the insult was post
renal.
Second we correct the fluid and electrolyte imbalance through the proper pharmaceutical
support. What was done to our patient was the anemia correction through the
transfusion and electrolyte correction through oral potassium supplementation and MgSO
drips.
Lastly, there are other steps to the management. We need to resort to the following
steps for supportive management to better the prognosis of the patient. We will need
nutritional support to prevent hypoglycemia and prevent starvation ketoacidosis and
protein catabolism. We will need blood transfusion in the case of anemia as well as DVT
prophylaxis. When worse comes to worst, we will have to be open to the idea of dialysis
when medical management fails to controls the complications of AKI.
With regards to discussing the context of our patient, we have to first understand the
implications of the disease in terms of the patients prognosis.
This figure depicts the different renal consequences of AKI. Starting with the arrow
pointing to the top, we have severe cardiac arrhythmia, muscle weakness, paralysis, and
depressed sensorium from Electrolyte Disturbances. Next patients with AKI can suffer
from protein catabolism, hepatic ischemia, hemodynamic instability from Acid Base
Disturbances. Also, patients with AKI tend to be uremic causing increased microvascular
permeability, bleeding diathesis and having impaired mental states.
The relationship between AKI and fluid overload is pretty simple. Oliguria leads to fluid
overload which leads to pulmonary edema which leads to right sided heart failure which
can lead to decreased cardiac output which can place the patient into a shock state.
Previously explained, we see that kidney injury can affect the lungs and the heart. But
we see in this figure that AKI also affects the brain, liver, GI tract, and bone marrow.
Patients with AKI can develop coagulation disorders, hypokalemia, liver failure, and even
cerebral edema.
This systemic approach to AKI is reflected in other short-term effects. An episode of AKI
confers an increased risk of further episodes of AKI, perhaps through the mechanisms
described, the subsequent development of acute kidney disease (AKD), and ultimately
the risk of CKD.
In terms of long term effects of AKI, this figure explains that AKI will eventually lead to
ESRD if the short term effects are not properly managed. Recurrent AKI leads to
diminishing renal function that would lead to elevated blood pressure and cardiovascular
events which could lead to renal hyperfiltration, progressive nephrite loss and
glomerulosclerosis. In general, damage to a single nephron can cause a chain reaction
which can eventually lead to ESRD.
Most common long term sequelae of AKI would be RRT or even death. The data before
you are the outcomes of the different studies on AKI with their corresponding mortality
rates, and more often than not the outcomes are grim, meaning to say there are often
mortalities than morbidities.
Rather than the outcome of AKI being a simple binary endpoint of dialysis or not, or
survival or not, the picture is much more complex and worrying than that. The PICARD
study, an observational multi-centre study of 618 critically ill patients showed that 40 %
went on to develop sepsis after AKI had occurred. Compared to those without
sepsis but with AKI, there was an increase in length of stay, risk of dialysis
requirement and mortality Even if our patient has not developed SEPSIS during her
admission, we believe that this knowledge is an important point of learning for us
medical practitioners.
Various mechanisms have been proposed to explain this phenomenon including reduced
pro-inflammatory cytokine clearance and impaired neutrophil function. It follows that
such sequelae will have consequences over and above that of changes in urine output
and serum creatinine, and, as such, AKI is associated with multi-system effects. As seen
in this figure, the decreased clearance of several pro-inflammatory cytokines have
different effects to different organs the net effect being to increase inflammation
systematically.
The Economic Burden of AKI is all to real. The data before you was derived from the
annual journal of surgery last 2014 which shows the prevalence of AKI as well as the
increasing costs and length of stay associated with AKI. From the data we can conclude
that Acute kidney injury is an all too common complication, afflicting between 7 percent
and 18 percent of all hospitalized patients and up to 50 % of critically ill patients. The
condition is associated with a 10-fold increase in hospital mortality rates and a higher
rate of chronic kidney disease among post-op patients
The effect of AKI would result into increased length of hospital stay, Hospital Costs,
Remission into disease in the next 30 days, and hospital mortality rates. All of which is
directly proportional to the severity of the kidney injury.
For a public health update, due to the increasing number of patients requiring
hemodialysis, the Philippine Health Insurance Corporation has reacted to this demand by
doubling the number of days covered in the PhilHealth Dialysis package. From 45 session
coverage, now the package covers 90 sessions. The question now would be even with
the doubling of allotted sessions, would the quality of service change? What would the
effect of this change be on the HD centers accredited by PhilHealth?
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