A 55-year-old male presented with pain and swelling in his left foot and lower leg along with abdominal pain and drowsiness. Examination revealed tachycardia, hypotension, tachypnea, and abdominal tenderness. Laboratory findings were consistent with diabetic ketoacidosis (DKA): hyperglycemia, ketonemia, and metabolic acidosis. The patient was diagnosed with DKA likely precipitated by infection and treated with insulin, intravenous fluids, potassium supplementation, and monitoring of electrolytes and glucose levels.

1.  A 55 year male patient was brought by
relatives to the ESR with c/o pain and
swelling over lt foot extending upto below
knee.Pt also c/o abdominal pain and
drowsiness since two days.
 O/E:- P:120 bpm, BP:-100/60 mmHg, RR:-
30cpm, Per abdomen exam reveals
tenderness.

3.  General and systemic including airway exam.
 Routine blood investigations:
 Hb:10gm%, CBC: 20200/cu.mm, RFTs &
LFTs: WNL, RBS: 320mg/dl,
 Serum. electrolytes:- Sr. Na:130mEq/l, Sr. K:
5mEq/l
 Chest Xray: increased BVM, ECG: NSR, Urine
routine microscopy;

4.  Special investigations:
 Serum and urine ketones: ++,
 ABG:- pH:7.25, pO2:90, pCO2:28, Sr
bicarbonate:15, BE:-9, SO2:97%
If a classic triad of DKA i.e hyperglycemia,
ketonemia and metabolic acidosis is
seen,diagnosis

5.  A state of absolute or relative insulin
deficiency aggravated by ensuing
hyperglycemia, dehydration, and acidosis-
producing derangements in intermediary
metabolism, including production of
serum acetone.
 Can occur in both Type I Diabetes and
Type II Diabetes
 In
type II diabetics with insulin
deficiency/dependence
 The presenting symptom for ~ 25% of Type
I Diabetics

7.  Stressful precipitating event that results
in increased catecholamines, cortisol,
glucagon.
 Infection (pneumonia, UTI)
 Alcohol, drugs
 Stroke
 Myocardial Infarction
 Pancreatitis
 Trauma
 Medications (steroids, thiazide diuretics)
 Non-compliance with insulin

8.  Polyuria
 Polydypsia
 Blurred vision
 Nausea/Vomiting
 Abdominal Pain
 Fatigue
 Confusion
 Obtundation

9.  Tachycardia
 Dehydration / hypotension
 Tachypnea / Kussmaul respirations /
respiratory distress
 Abdominal tenderness (may resemble acute
pancreatitis or surgical abdomen)
 Lethargy / obtundation / cerebral edema /
possibly coma

10.  INSULIN
 Administer short-acting insulin: IV (0.1
units/kg) or IM (0.3 units/kg),
 then 0.1 units/kg per hour by continuous IV
infusion;
 Increase 2- to3-fold if no response by 2–4 h.
 If initial serum potassium is < 3.3
meq/l,correct K level while giving insulin to
prevent dangerous hypokalemia.
 Expected fall is 50-100 mg/h
 Transition into SQ when:
A. Plasma glucose is less than 250 mg/dl
B. DKA has resolved (usually less than 12 hs)
C. Patient is tolerating PO

11. FLUID
1. Deficit is around 6-8 L – need NOT to replace
all of it with IV fluid
 Replace fluids: 2–3 L of 0.9% saline over first
1–3 h (10–15 mL/kg per hour);
 Subsequently 0.45% saline at 150–300mL/h;
 Change to 5% glucose and 0.45% saline at
100–200 mL/h when plasma glucose reaches
250 mg/dL (14 mmol/L).
 Watch BP, pulse, BUN/creatinine and urinary
output.
 Use plasma expanders/blood if in shock and
does not respond quickly to saline.

12. ELECTROLYTES
1. The critical is K
2. There is always a deficit, but blood levels
may be low, normal or high
3. Frequent EKG and serum levels are
mandatory
4. Initially IV may be the only way to
administer K but remember that once PO is
re-established, K can be given orally.
 Factors reducing serum K+
 􀁺 Rehydration → ↑ urinary secretion of K+
 􀁺 Insulin administration moves K+ from
extracellular to intracellular.

13. Replace K+:
 10 meq/h when plasma
K+ < 5.5 meq/L, ECG
normal, urine flow and SERUM K
LOW (<3.5)
Rate hour
40 Meq
Normal (3.5-5.0) 20 Meq
normal Cr. Normal, pH <7.0 or
EKG changes
40 Meq
High (>5.0) Hold until level
 40–80 meq/h when High (>5.0) pH < 7.0
normal
10-20 meq
or EKG changes
plasma K+ < 3.5 meq/L
or if bicarbonate is
given.

14. BICARBONATE
1. Usually NOT necessary
2. It may even be dangerous and
precipitate hypokalemia, cerebral
acidosis and cardiac dysfunction
3. For very severe acidosis (pH <6.9) use
very small amounts enough to elevate
pH to 7.0

15. PHOSPHATE AND OTHER ISSUES
Supplementation only advised if Serum
phosphate conc <1.0mg/dl or in the
presence of anemia, cardiac
dysfunction.
If needed, 20-30 mEq/l potassium
phosphate can be given.
Broad spectrum antibiotic coverage is
required.

16.  Measure capillary glucose every 1–2 h;
 electrolytes (especially K+, bicarbonate, phosphate) &
anion gap every 4 h for first 24 h.
 Monitor BP, pulse, respirations, mental status, fluid intake
and output every 1–4 h.
 Assess patient:
 What precipitated the episode (noncompliance, infection,
trauma, infarction, cocaine)?
 Initiate appropriate workup for precipitating event
(cultures, CXR, ECG).
 Continue above until patient is stable, glucose goal is 150–
250 mg/dL, and acidosis is resolved.
 Insulin infusion may be decreased to 0.05–0.1 units/kg/hr.

17.  Cerebral edema  Pulmonary Edema
First 24hrs and Hypoxemia
 Mental status changes
 Tx: Mannitol
 Iatrogenic
 May require intubation
hypoglycemia and
with hyperventilation hypokalemia
 Shock
 If not improving with
fluids r/o MI
 Vascular
thrombosis
 Severe dehydration
 Cerebral vessels
 Occurs hours to days
after DKA

18.  With a central line already in situ, patient is
taken inside the O.T. after checking
starvation and high risk consent.
 Adequate amount of crossmatched blood is
kept ready.
 The standard monitors attached. HGT,CVP
and urine output monitoring is essential.
 IV fluid is attached.

19.  Low dose unilateral sub arachnoid block can
be given using 0.5%(H) Inj.Bupivacaine and
Inj. Fentanyl as additive making a total
volume of 1.2-1.4cc.
 Excellent analgesia.no need to use NSAIDS or
opiods intra op.
 Hypoglycemia & hyperglycemic coma can be
detected early.
 Avoidance of ETT & resultant infection.

20.  Disadvantages:
 Inadvertant higher level of block can result
in hypotension complicated by autonomic
neuropathy in DM.
 Sympathetic blockade can impair control of
insulin secretion.

21.  Femorosciatic nerve block can be given which
helps prevent hypotension and also provides
superior intra and post op analgesia

22.  Epidural anaesthesia either single shot or
catheter in situ can be used to avoid
hypotension and also for post op pain relief.
 Disadvantage includes risks of infection and
vascular damage.

23.  For small ulcers confined to foot, ankle block
using Inj. Bupivacaine and Inj Lignocaine can
be given.

24. Aspiration prophylaxis is given with antacid
and antiemetic.
 Rapid sequence induction should be done in
case of inadequate starvation or autonomic
neuropathy(gastroparesis).
 Muscle relaxant: Rocuronium should be used
instead of Sch i/c/o hyperkalemia
 After induction, Inj.midazolam and
opiod(preferably fentanyl) is given in titrated
doses for analgesia and sedation.

25.  Maintenance: oxygen & nitrous oxide and
sevoflurane or Isoflurane.
 Reversal:routine reversal
 Extubation: after adequate recovery of
airway reflexes.
 Post op monitoring: blood sugar level,serum
and urine ketones, serum electrolytes