DR G F KEJEKGABO (MBBS) (UB)

Supervised by : DR CHABAESELE
OUTLINE

• • Physical
• Background • History
Demographics Exam

• • • Teaching
• Assessment
Investigations Management Slides
DEMOGRAPHICS
•K K
• 43/M
• Resident of Molepolole and Kopong
• Father of 2, married
• Truck driver
• Alcohol: occasionally< CAGE –
• No hx of smoking
MEDICAL BACKGROUND
• RVD neg
• HTN since 3 years, sub-optimal controlled, on HCT 25 OD & Nif 30 OD
nil documented TODs
• Newly dx T2DM, since a month back, poorly controlled, recent
HBA1C>14.5, on Metformin 500mg BD, nil documented TOD
Recently screened for Retinopathy: N fundoscopic exam
HISTORY
• PC: 1 week of progressively worsening GBW
• HPI; previously well until a week and a half back, started to
experience GBW which is progressively worsening, interferes with day
to day activity
• a/w: 2 day history of vomiting post feeds, non-projectile, non-bloody,
non bilious, mostly constituted of food particles, patient felt nauseas
before the vomiting episodes, reported around 5-6 episodes on day of
admission.
• New onset
HISTORY
• Nil infections(cough, diarrhea, vomiting, dysuria), surgery, trauma,
myocardial infarction, burns, heatstroke
• Nil glucocorticoid therapy, cocaine use, + alcohol abuse
• nil toxin ingestion, started on Metformin recently,
• reported poor feeding and reduced appetite,
• Nil bloating, early satiety or feeling unusually full.
• Nil tingling sensation on extremities
HISTORY
• + Increased WOB, nil cough, fevers nor chills, no sick contacts/ Tb
contacts, nil chest pains radiating to jaw/ left arm, nil diaphoresis, nil
PND, orthopnea, nil limb swelling, nil hx of trauma
• Of late: + hx of polydipsia, polyphagia, polyuria, mild abdominal pains,
denies visual changes, pins and needles, oliguria, hemiparesis, angina,
claudication, ED, foot ulcers nor any rashes
• Reports poor dietary adherence, nil conflicts at home
• +fam hx: DM, HTN
HISTORY
• ROS; unremarkable
• Past medical: as above
• Past surgical: nil
• Drug hx: as above
• Social and personal history: as above
PHYSICAL EXAM
• General exam: awake, alert, hyperventilating, obese looking
mid aged male, lying on bed with FMO2 at 3L next to patient,
with IV line insitu
JACCOLD-, mild-mod dehydration
• v/s: BP:161/94 P:101 RR:32 Sats: 96 on RA Temp:36.0
RBS:29.9 Wt: 99
• HEENT: normocephalic, atraumatic, +acanthosis nigricans
• CVS: RRR, CRT<3s, quiet precordium, PMI 5ICS LMCL, S1S2
normal, no murmurs audible
PHYSICAL EXAM
• Abdo: +fat distension, nil scars, nil stigmata of CLD, soft non-
tender, nil hepatosplenomegaly, no masses, tympanic and
normal B/S
• Resp: in resp distress, speaking in syllables, tachypnic, equal
chest wall rise, GAEB, resonant to percussion, vesicular
breath sounds nil added sounds, no creps nor wheezes
• CNS: GCS 15/15, O*3, PEARL, nil meningism, CN intact,
motor 4/5 globally, normal reflexes, sensation and nil
cerebellar signs
INVESTIGATONS
ABG & Dipstick ABG & Dipstick FBC/RFT LFT
(30/11/23)- AnE (30/11/23)- AnE
PH: 7.08 PH: 7.25 WBC: 8.3 T Bil: 8.5
HCO3:9.3 HCO3: 10.6 HB: 17 D Bil: 2.3
PCO2:31.5 PCO2: 24.5 MCV: 85.3 AST: 22
AG: HIGH AG: 26.1 PLT:283 ALP: 117
BE: -19.2 BE: -14.8
K: 4.3 K: 4.24 Na: 136 ALT: 25
Na: 137 Na: 137
KET 4+ NIT- KET 3+ NIT- K: 5.7 GGT: 38
GLU 2+ LEU +/- GLU 2+ LEU +/- U: 13.6 T Prot: 87
PROT+/- PROT+/- Cr: 107 Alb: 50.0
SUMMARY
• 43/M, RVD neg, HTN on rx, sub-optimal control to r/o TOD, newly
diagnosed with T2DM, poorly controlled with HBA1c of > 14.5, came
in with GBW, vomiting, increased WOB and mild generalized
abdominal pains, tachypneic, hyperglycemic with High Anion Gap
Metabolic Acidosis
SUMMARY
• 43/M, RVD neg, HTN on rx, sub-optimal control to r/o TOD, newly
diagnosed with T2DM, poorly controlled with HBA1c of > 14.5, came
in with GBW, vomiting, increased WOB and mild generalized
abdominal pains, tachypneic, hyperglycemic with High Anion Gap
Metabolic Acidosis

DDx? DKA vs HHS

HAGMA—ddx
SUMMARY
• 43/M, RVD neg, HTN on rx, sub-optimal control to r/o TOD, newly
diagnosed with T2DM, poorly controlled with HBA1c of > 14.5, came
in with GBW, vomiting, increased WOB and mild generalized
abdominal pains, tachypneic, hyperglycemic with High Anion Gap
Metabolic Acidosis

DDx? DKA vs HHS

HAGMA—ddx
 DKA  Renal Failure  Methanol
 AKA  Lactic (D & L)  Propylene glycol
 SKA  Aspirin  Oxoloprolinemia
 Metformin  Ethanol  Ethylene glycol
ASSESSMENT
Impression:
Severe Diabetic Keto-Acidosis with moderate dehydration
• ?precipitating factors: most likely poor control
• complicated by: Acute Kidney Injury; pre-renal/ATN
Metabolic Phenotype: MUO
• Obesity
• Abdominal obesity
• Hypertension
• Hyperglycemia
• Dyslipidemia.
MANAGEMENT
• Patient initiated on DKA protocol in AnE
• Plan on admission- Out of DKA
Admit to MMW
Initiate Sliding Scale
Lipid profile
ECG/UMCS
Dietician and Endoncrinology consults
Metformin 1 g
Monitor RBS and BPs
IVF
Hold nephrotoxic drugs
Monitor UO
WARD PROGRESS
Sinus rhythm
Intermediate
axis

Source: Patient
Records
 WARD PROGRESS

Source: IPMS
 WARD PROGRESS

Source: IPMS
WARD PROGRESS
VBG(01/12/23)

PH:7.368
AG: 12
HCO3: 22.0

PC02: 39.2

BE:-2.9

Na: 141

K: 3.7

CL:104

Source: IPMS
 SUBJECTIVE OBJECTIVE ASSESMENT PLAN
DAY 1 GBW, intermittent RBS: 17.1 DKA resolved, Protaphane 8 IU
headache and BP:134/87 hyperglycemia, AKI Clexane 40 mg SC
abdominal pain P;89 T;36.4 Monitor RBS
DAY 4 Feeling better, RBS: 16.9 BP: T2DM, uncontrolled, Artovastatin
GBW resolved 138/91 P:77 hyperlipidemia, AKI FBC/RFT/LFT/CMP/KUB
T: 36.0 ECG? Ischemic Î Protaphane dose to 10IU
changes with RAD SC OD, INCREASW IVF,
?HIT:stop Heparin
F/U dietician
Day 5 Feeling better, nil RBS: 16.3 DM uncontrolled, Seen by endocrinologist
vomiting, BP: 136/89 HTN controlled, Actrapid 10 IU stat
headaches nor p:80 T: 35.0 hyperlipidemia Increase PO water intake
abdo pain Increase Protaphane to 14
IU
 SUBJECTIVE OBJECTIVE ASSESMENT PLAN

DAY 6 Nil complaints RBS:13.9 DM, HTN, Increase Protaphane

BP: 132/70 P:81 hyperlipidemia, to 18IU
T:36.0 AKI resolved, Metformin to
DKA resolved 2.5g/day
Monitor RBS
Seen by dietician
DAY 7 Nil complaints RBS: 8.8 BP: DM controlled, Patient discharged
129/80 P:77 T: 36.0 HTN controlled, on Protaphane 18IU,
hyperlipidemia, metformin 2.5g/day
AKI resolved, HCT 12.5mg OD, /Nif
DKA resolved 60 OD
Artovastatin 40 OD
DKA

Source: SLH DKA Management Protocol

ETIOLOGY
Increased insulin demands and insufficient/treatment failure

Newly diagnosed cases

Insulin omission
Poor diet
Poor metabolic control
Previous episodes of DKA
ETIOLOGY
Infections such as gastroenteritis, UTI

Challenging social and family circumstances

Peripubertal and adolescent girls

Failures in insulin pump therapy

Psychosocial (dysfunctional family, anxiety disorder, depressive disorder)

Sleep disorder
PATHOPHYSIOLOGY
Osmotic diuresis and hypovolemia
• Insulin-deficient state  hyperglycemia
• Hyperglycemia osmotic diuresis  volume depletion

Insulin deficiency → hyperglycemia → hyperosmolality →

osmotic diuresis and loss of electrolytes → hypovolemia
+/- →AKI
PATHOPHYSIOLOGY
Metabolic acidosis with increased anion gap
• Insulin deficiency  lipolysis
• Ketones (acetoacetic acid and beta-hydroxybutyric acid) lead to
metabolic acidosis
• Serum bicarbonate buffers the acidic ketones thus high AG

Insulin deficiency → ↑ lipolysis → ↑ free fatty acids → hepatic

ketone production (ketogenesis) → ketosis → bicarbonate
consumption (as a buffer) → anion gap metabolic acidosis
PATHOPHYSIOLOGY
Intracellular potassium deficit
• Hyperglycemic hyperosmolality  potassium and watershifts from
intracellular to the extracellular space and is lost in the urine.
• Insulin normally promotes cellular potassium uptake but is absent in
DKA, compounding the problem.
• A total body potassium deficit develops in the body, although serum
potassium may be normal or even paradoxically elevated.
Insulin deficiency → hyperosmolality → K+ shift out of cells + lack of
insulin to promote K+ uptake → intracellular K+depleted → total body
K+ deficit despite normal or even elevated serum K+
CLINICAL
INVESTIGATIONS
1. Blood glucose
2. Blood ketones
3. Urine dipstick
4. Urea and electrolytes, CMP
5. Blood gas
6. ECG (for all adults)
7. Other investigations only if indicated
• Full blood count
• Blood culture
• Urine culture
• LP
• CXR
GOALS OF TREATMENT

3. Correct
1. Correct 2. Correct acidosis
electrolyte
dehydration and reverse ketosis
imbalance

4. Monitor for
5. Identify and treat
complications of
any precipitating
DKA and its
event
treatment
RESUSCITATION

Airway Breathing
Circulation Disability Airway protection, if 2 large bore IV
Exposure (ABCDE) required cannulas
resuscitation

Cardiac monitor Full clinical

Glasgow coma scale
placement assessment
CORRECTION OF DEHYDRATION
• Assess the severity of
dehydration
• Initial IVF should be given until
the patient is euvolemic
• Give isotonic solution preferably
Normal Saline
• Fluid replacement should be
given over 24 to 48 hours
Source: Mahalapye District Hospital DKA
Management Protocol
POTASSIUM REPLACEMENT
• Correct K first then start
insulin
• Never give KCL as a push
• Never add >40mmol of KCL
in a 1L of IVF
• Never exceed rate of
0.4mmol/kg/h Source: SLH DKA Management Protocol
• Recheck K every 2-4 hours
(at minimum twice daily)
CORRECTION OF ACIDOSIS
INSULIN DRIP 

SUBCUTANEOUS
INSULIN


Insulin used to treat

acidosis, not
hyperglycemia

Insulin should be
maintained until
resolution of ketosis

If no pump or IV insulin
infusion is not possible
give 1-2 hourly
SC insulin
MONITORING
TRANSITION TO SC INSULIN
PRESCRIBING SC INSULIN
SLIDING SCALE

Source: SLH DKA Management Protocol

Source: SLH DKA Management Protocol
MANAGEMENT

Source: SLH DKA Management Protocol

 ASSIGNMENTS

• DKA VS HHS
• DM SLIDING SCALE VS
CORRECTION SCALE
• ANTI DIABETIC THERAPY

SOURCE: GOOGLE
REFERENCES
• Scottish Livingstone Hospital DKA Protocol
• Management of Diabetic Ketoacidosis Protocol: Mahalapye District
Hospital. Mosalakatane et al, 2019
• Uptodate
• Amboss
• Goguen J, Gilbert J, Hyperglycemic Emergencies in Adults, 2018
Clinical Practice Guidelines, Chapter 15, Diabetes Canada
• Westerberg DP. Diabetic Ketoacidosis: Evaluation and Treatment. Am
Fam Physician. 2013; 87(5): p.337-346. pmid: 23547550.
THANK YOU