1.0 sugar, low blood pH, and ketoacids in

1.0 INTRODUCTION

Diabetic
ketoacidosis (DKA) is a potentially life-threatening complication of diabetes
mellitus. Signs and symptoms may include vomiting, abdominal pain, deep gasping
breathing, increased urination, weakness, confusion, and occasionally loss of
consciousness. A person’s breath may develop a specific smell. Onset of
symptoms is usually rapid. In some cases people may not realize they previously
had diabetes.

DKA
happens most often in those with type 1 diabetes, but can also occur in those
with other types of diabetes under certain circumstances. Triggers may include
infection, not taking insulin correctly, stroke, and certain medications such
as steroids. DKA results from a shortage of insulin, in response the body
switches to burning fatty acids which produces acidic ketone bodies. DKA is
typically diagnosed when testing finds high blood sugar, low blood pH, and
ketoacids in either the blood or urine.

The
primary treatment of DKA is with intravenous fluids and insulin. Depending on
the severity, insulin may be given intravenously or by injection under the
skin. Usually potassium is also needed to prevent the development of low blood
potassium. Throughout treatment blood sugar and potassium levels should be
regularly checked. Antibiotics may be required in those with an underlying
infection. In those with severely low blood pH, sodium bicarbonate may be
given, however its use is of unclear benefit and typically not recommended.

 

 

 

 

 

 

 

 

 

2.0 CASE STUDY

 

Mr.
Saifuddin Bin Ab Rahman, 45 years old with underlying Diabetes Mellitus for
the past 8 years ago, on medication metformin and gliclazide. He also had hypertension
since 4 years ago, on one antihypertensive medication but noncompliance to
medication. Patient under Klinik Kesihatan Tawau follow up. Patient presented
to ED Hospital Sungai Buloh with complaints of upper abdominal pain for four
days and worsening today. The pain score was 7/10. Not related to meal and
non-radiating. Patient had complaining of vomiting two episodes since today
with food content, no biles and no blood. Patient also having shortness of
breath today night, thus came in to ED. Patient bowel open and urine output is
normal. Patient had reduced oral intake since yesterday. Otherwise, patient
denied of fever, diarrhoea, chest pain, palpitation, slurred speech, body
weakness, UTI symptoms and URTI symptoms. Patient actually travelled from Tawau
Sabah visiting relatives. However his medication was finished. So he not takes his
medication for the past one week.

 

On examination upon
arrival in ED, the patient was drowsy;
GCS full, peripheries were warm, good pulse volume, capillary refill time less
than 2 seconds, rapid and deep breathing. Patient looks lethargic. The tongue
was moist. His vital signs were Temperature was 37 Celcius, Pulse rate was 125
bpm, Respiration rate was 30/min, Blood pressure was 137/86 mmHg, MAP: 99 mmHg
and Sp02 was 98% under room air. Auscultation on lungs showed equal and clear
air entry. Cardiovascular system showed dual rhythm no murmur. Examination on
abdomen showed soft tenderness over epigastric, right hypochondriac and left
hypochondriac region.

 

Investigation that had
been done to Mr. Saifuddin includes Full Blood Count (FBC). The results were Hb
20.6 / Hct 58 / WCC 16.7 / Platelet 329. The result of Venous Blood Gases were pH
7.037 / HC03 8.4 / lactate 5.3 / BE -21 / glucose 54 / Potassium (K) 4.9 / Sodium
(Na) 129. The urine ketone was 4.8. Capillary blood glucose was high. ECG
showed sinus tachycardia. The impression
for Mr Saifuddin was Diabetic Ketoacidosis secondary to noncompliance to
medication.

 

The plan management for
this patient at resus with weight of 84 kg were High flow mask 15L/min. IV drip
normal saline 20cc/kg/hour. IV infusion insulin 0.1mg/kg/hour. Insertion of CBD.
Sent for chest X-ray. Monitor the vitals sign and Dextrostix hourly.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

3.0 DISCUSSION

 

From the case study above, it is clear
that Mr. Saifuddin is underlying of hypertension and diabetes mellitus. Patient
actually travelled from Tawau Sabah visiting relatives. However his medication
was finished. So he not takes his medication for the past one week. This
considers the patient has miss medication leads to serious complication which
is diabetic ketoacidosis (DKA). The symptoms like abdominal pain, vomiting and
loss of appetite that he had can consider that he had complication of his
diabetes.

 

Diabetic ketoacidosis
(DKA) is a complex disordered metabolic state characterised by hyperglycaemia,
acidosis, and ketonaemia. DKA usually occurs as a consequence of absolute or
relative insulin deficiency that is accompanied by an increase in
counterregulatory hormones (ie, glucagon, cortisol, growth hormone,
epinephrine). This type of hormonal imbalance enhances hepatic gluconeogenesis
and glycogenolysis resulting in severe hyperglycaemia. Enhanced lipolysis
increases serum free fatty acids that are then metabolised as an alternative
energy source in the process of ketogenesis. This results in accumulation of
large quantities of ketone bodies and subsequent metabolic acidosis. Ketones
include acetone, 3-beta-hydroxybutyrate, and acetoacetate. The predominant
ketone in DKA is 3-betahydroxybutyrate (Caputo, D.G. 2010).

 

According to Kitabchi,
A.E.& Nyenwe, E.A. (2006), DKA consists of the biochemical triad of
ketonaemia/ ketonuria, hyperglycaemia, and acidaemia. From the above case
study, Mr. Saifuddin showed ketone in his urine as the result of urine ketone
was 4.8. Patient’s capillary blood glucose was high and from the result of
venous blood gas (VBG), the glucose was 54. Patient is hyperglycaemia. The
result of VBG also showed the patient had acidosis which the pH was 7.037 and
HC03 was 8.4. From all the investigation carried out to Mr. Saifuddin, it
showed that he is diagnosed with Diabetes Ketoacidosis and must be treating
promptly.

 

There are several
mechanisms responsible for fluid depletion in DKA. These include osmotic
diuresis due to hyperglycaemia, vomiting commonly associated with DKA, and
eventually, inability to take in fluid due to a diminished level of
consciousness. Electrolyte shifts and depletion are in part related to the
osmotic diuresis. Hyper and hypokalaemia need particular attention.

 

            According
to Devalia, B. (2010) the therapeutic goals of DKA management include
optimization of volume status, hyperglycemia and ketoacidosis, electrolyte
abnormalities; and potential precipitating factors. The majority of patients
with DKA present to the emergency room. Therefore, emergency physi­cians should
initiate the management of hyperglycemic crisis while a physical examination is
performed, basic metabolic parameters are obtained, and final diagnosis is
made. Several important steps should be followed in the early stages of DKA
management. First of all, collect blood for metabolic profile before initiation
of intravenous fluids. Then, infuse 1 L of 0.9% sodium chloride over 1 hour
after drawing initial blood samples. Next, ensure potassium level of >3.3
mEq/L before initiation of insulin therapy (supplement potassium intravenously
if needed). Lastly is initiate insulin therapy.

 

            Blood
glucose is routinely checked at the bedside, but portable ketone meters now
also allow bedside measurement of blood ketones (3-betahydroxybutyrate). This
is an important advance in the management of DKA (Sheikh-Ali, 2008). The
resolution of DKA depends upon the suppression of ketonaemia, therefore
measurement of blood ketones now represents best practice in monitoring the response
to treatment. Access to blood gas and blood electrolyte measurement is now
relatively easy and available within a few minutes of blood being taken.
Therefore glucose, ketones and electrolytes, including bicarbonate and venous
pH should be assessed at or near the bedside.

 

            The
most important initial therapeutic intervention in DKA is appropriate fluid
replacement followed by insulin administration. The main aims for fluid
replacement are restoration of circulatory volume, clearance of ketones and
correction of electrolyte imbalance. For example, an adult weighing 70kg
presenting with DKA may be up to 7 litres in deficit. This should be replaced
as crystalloid. In patients with kidney failure or heart failure, as well as the
elderly and adolescents, the rate and volume of fluid replacement may need to
be modified. The aim of the first few litres of fluid is to correct any
hypotension, replenish the intravascular deficit, and counteract the effects of
the osmotic diuresis with correction of electrolyte disturbance (Nyenwe, E.A.
& Kitabchi, A.E. 2011).

 

            For Insulin therapy a fixed rate calculated
on 0.1 units/ per kilogram infusion is recommended. It may be necessary to estimate
the weight of the patient. Insulin has the following effects such as
suppression of ketogenesis, reduction of blood glucose and correction of
electrolyte imbalance. The metabolic treatment targets include reduction of the
blood ketone concentration by 0.5 mmol/L/hour, increase the venous bicarbonate
by 3 mmol/L/hour, reduce capillary blood glucose by 3 mmol/L/hour, potassium
should be maintained between 4.0 and 5.0 mmol/L. If these rates are not achieved
then the fixed rate IV insulin infusion rate should be increased (Randall, L.,
Begovic, J., Hudson, M., et al. 2011).

 

According to Umpierrez,
G.E., Smiley, D. & Kitabchi, A.E. (2012) the management of intravenous
glucose concentration should be focussed on clearing ketones as well as normalising
blood glucose. It is often necessary to administer an intravenous infusion of
10% glucose in order to avoid hypoglycaemia and permit the continuation of a
fixed rate IV insulin infusion to suppress ketogenesis. Introduction of 10%
glucose is recommended when the blood glucose falls below 14 mmol/L. It is important
to continue 0.9% sodium chloride solution to correct circulatory volume. It may
be necessary to infuse these solutions concurrently. Glucose should not be discontinued
until the patient is eating and drinking normally.

 

 

 

 

 

 

 

 

 

 

 

 

4.0  NURSING CONSIDERATION

 

An important part of the
plan is the nursing diagnosis. It is made based on the assessment of the
medical history, symptoms, drugs administered and clinical assessment. In this
case, the condition due to diabetic ketoacidosis is a fluid volume deficit,
metabolic acidosis, excessive blood glucose levels, high potassium levels,
dehydration, along with imbalances in nutrition, infection related to the influenza
and fatigue. The key nursing diagnoses include high blood glucose related to
insulin deficiency as manifest by diabetic ketoacodosis. Besides, dehydration
related to hyperglycemia as manifest by frequent urination, weakness and dry
skin also important in nursing diagnosis. Other nursing diagnosis potassium imbalance
related to osmotic diuresis as manifest by unstable vital signs, cramps and
muscle weakness. Lastly, metabolic acidosis related to ketones presence in
blood as manifest by kussmul’s breathing, nausea, confusion and drowsiness.

The assessment
would include the airway, breathing, circulation (dehydration) and the
neurological state. There is an osmotic diuresis related to hyperglycemia
causing excessive gastric losses in the form of vomiting, abdominal pain and
diarrhea, and lowered intake of food (nausea and sub-consciousness). The
sensory perception of the patient is also altered due endogenous chemical
alterations. Evidence for making the nursing diagnosis is done based on the
presence of symptoms/features such as great output of urine, diluted urine,
excessive thirst, sudden loss of body weight, poor food intake, diarrhea and
vomiting, altered neurological state, rise in the ketone levels in the blood
and the urine, lowered blood pressure and increased heart rate, Kussmaul’s
respiration (deep and rapid breathing), and dry and cracked skin with poor
turgor.

 

 

 

 

 

 

 

 

5.0 SUMMARY

Hyperglycemia and
ketosis in diabetic ketoacidosis (DKA) are the result of insulin deficiency and
an increase in the counterregulatory hormones glucagon, catecholamines,
cortisol, and growth hormone. Three processes are mainly responsible for
hyperglycemia: increased gluconeogenesis, accelerated glycogenolysis, and
impaired glucose utilization by peripheral tissues. This might also be
augmented by transient insulin resistance due to hormone imbalance, as well as
elevated free fatty acids.

DKA is most commonly precipitated by infections. Other factors
include discontinuation of or inadequate insulin therapy, pancreatitis,
myocardial infarction, cerebrovascular accident, and illicit drug use. The
diagnostic criteria of DKA, established by the American Diabetic Association,
consists of a plasma glucose of >250 mg/dL, positive urinary or serum
ketones, arterial pH of <7.3, serum bicarbonate <18 mEq/L, and a high anion gap. The key diagnostic feature of DKA is elevated circulating total blood ketone concentration. Hyperglycemia is also a key diagnostic criterion of DKA; however, a wide range of plasma glucose levels can be present on admission.                               References   Caputo, D.G., Villarejo, F., Valle, G.B., Díaz, A.P., Apezteguia, C.J. (2010). Hydration in diabetic ketoacidosis. What is the effect of the infusion rate? Medicina (B Aires) 2010;57(1):15–20. Devalia, B. (2010). Adherance to protocol during the acute management of diabetic ketoacidosis: would specialist involvement lead to better outcomes? Int J Clin Pract. 64(11):1580–1582. Gosmanov, A.R., Umpierrez, G.E., Karabell, A.H., Cuervo, R., Thomason, D.B. (2014). Impaired expression and insulin-stimulated phosphorylation of Akt-2 in muscle of obese patients with atypical diabetes. Am J Physiol Endocrinol Metab. 287(1):E8–E15. Kitabchi, A.E., Nyenwe, E.A. (2006). Hyperglycemic crises in diabetes mellitus: diabetic ketoacidosis and hyperglycemic hyperosmolar state. Endocrinol Metab Clin North Am. 35(4):725–751. Kitabchi, A.E., Umpierrez, G.E., Murphy, M.B., Kreisberg, R.A. (2006). Hyperglycemic crises in adult patients with diabetes: a consensus statement from the American Diabetes Association. Diabetes Care. 29(12):2739–2748.  Nyenwe, E.A., Kitabchi, A.E. (2011). Evidence-based management of hyperglycemic emergencies in diabetes mellitus. Diabetes Res Clin Pract. 94(3):340–351. Randall, L., Begovic, J., Hudson, M., et al. (2011). Recurrent diabetic ketoacidosis in inner-city minority patients: behavioral, socioeconomic, and psychosocial factors. Diabetes Care. 34(9):1891–1896. Sheikh-Ali, M., Karon, B.S., Basu, A., et al. (2008). Can serum beta-hydroxybutyrate be used to diagnose diabetic ketoacidosis? Diabetes Care. 31(4):643–647.  Umpierrez, G.E., Smiley, D., Kitabchi, A.E. (2012). Narrative review: ketosis-prone type 2 diabetes mellitus. Ann Intern Med. 144(5):350–357.

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