In: Nursing
Mr. L is a 58-year-old man who is recovering in the orthopedic unit of the hospital from a right total knee replacement of two days ago. Mr. L has type 1 diabetes and was diagnosed with the condition at 12 years of age. He has been managing his illness with blood glucose checks 4 times a day: before meals and once at bedtime. He currently takes Humulin-R on a sliding scale based on his glucose results. He weighs 315 lbs. and has developed osteoarthritis in both knees, requiring surgical replacement of the knee joint on the right side.
The nurse caring for Mr.L. enters his room at 8:15 AM for a morning assessment. She finds Mr. L lying in his bed awake, but his mental status is altered and there is a fruity odor to his breath. His vital signs are: HR 100bpm, RR 32/minute, BP 116/78 mm Hg. The nurse notes that his last blood glucose level was 156 mg/dl the previous night before bed and he received 2 units of insulin at that time, but he has not received his morning glucose check or any insulin yet today. A rapid bedside glucose check reveals a blood glucose level of 468 mg/dl. The nurse contacts the physician and upon further examination, Mr. L is diagnosed with diabetic ketoacidosis.
Mr. L complains of feeling very thirsty and that he can’t see very well because his vision is suddenly blurry. The nurse notes he has a large amount of clear urine in his catheter bag. She takes a sample of urine and it tests positive for ketone bodies.
The physician has given orders to administer 0.9% Sodium Chloride IV at 500 mL/hour for 1 hour, then 200mL/hour for the next 4 hours. The nurse is to start a drip of Regular insulin at 0>1mg/kg/hour. The physician has also added orders for lab work, including a metabolic profile and arterial blood gases. The metabolic panel results are: Na 135 mEq/L, K 3.2mEq/l, CL 95mmol/L, Ca 8.5mg/dl. The arterial blood gases results are as follows: ph 7.31, pCO2 20 mmHg, pO2 95 mmHg, HCO3 12 mmol/L
An hour after the insulin was started, the nurse checks Mr. L.’s blood glucose levels and notes it has decreased to 208 mg/dl. He appears more comfortable and his vital signs are: HR 92 bpm, RR 22/ minute, BP 116/70mm Hg, O2 saturation 95% on 2L of oxygen.
How surgery causes DKA
Hyperglycaemia following surgical and anaesthetic stress is a
well-established entity which might have undesirable clinical
consequences in known diabetics.The stress induced by surgery and
anaesthesia lead to the genesis of this event. Anaesthesia and
surgery cause stereotypical metabolic stress which provokes the
release of the catabolic hormones epinephrine, norepinephrine,
cortisol, glucagon and growth hormone. Insulin secretion and action
are however inhibited. Catecholamines stimulate gluconeogenesis and
glycogenolysis but inhibit glucose utilisation and insulin
secretion. Other effects include lipolysis and ketogenesis. In
addition to insulin resistance induced by circulating stress
hormones, surgical stress deleteriously affects pancreatic cell
function. Plasma insulin levels fall and insulin secretory
responses to glucose become impaired.
Kussmauls respiration in DKA
Kussmaul breathing is a deep and labored breathing pattern often
associated with severe metabolic acidosis, particularly diabetic
ketoacidosis.Kussmaul breathing is the body's attempt to blow off
as much carbon dioxide as possible in order to compensate for the
metabolic acidosis from DKA
Cause of presence of Ketones in urine in DKA.
The condition develops when the body can't produce enough insulin.
Insulin normally plays a key role in helping glucose
metabolism.Without enough insulin, the body begins to break down
fat as fuel. This process produces a buildup of acids in the
bloodstream called ketones and these are eventually excreted
through urine developing ketonuria.
cause of blurred vision
The blurry vision in DKA results from rapidly fluctuating glucose
levels, which cause fluid quantities in the eye to constantly
change due to change in osmolality.
Cause of poly uria and poly dipsia
Polydipsia or increased thirst is due to high blood glucose that
raises the osmolarity of blood and makes it more concentrated.
Polyuria or increased frequency of urination is due to excess fluid
intake and glucose-induced urination. Weight loss occurs due to
loss of calories in urine.
Need of fluid management
Fluid resuscitation is a critical part of treating patients with
DKA. Intravenous solutions replace extravascular and intravascular
fluids and electrolyte losses. They also dilute both the glucose
level and the levels of circulating counterregulatory hormones.
Potassium level in DKA
Potassium levels can fluctuate severely during the treatment of
DKA, because insulin decreases potassium levels in the blood by
redistributing it into cells via increased sodium-potassium pump
activity. A large part of the shifted extracellular potassium would
have been lost in urine because of osmotic diuresis.
ABG values in DKA
In patients with DKA, arterial blood gases (ABGs) frequently show
typical manifestations of metabolic acidosis, low bicarbonate, and
low pH (less than 7.3).
Cause of acidosis in DKA
Acidosis in DKA is due to the overproduction of β-hydroxybutyric
acid and acetoacetic acid. At physiological pH, these 2 ketoacids
dissociate completely, and the excess hydrogen ions bind the
bicarbonate, resulting in decreased serum bicarbonate levels.
Nursing action after stabilisation
Continuous monitoring of blood sugar level.
Monitor ketone level.
Monitor client's mental status.
Give a long acting insulin according to doctor's order to sustain
normoglycemia.