of 25 /25
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.

Diabetic ketoacidosis ppt

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Page 1: Diabetic ketoacidosis ppt

A 55 year male patient was brought by relatives to the ESR with co pain and swelling over lt foot extending upto below kneePt also co abdominal pain and drowsiness since two days

OE- P120 bpm BP-10060 mmHg RR-30cpm Per abdomen exam reveals tenderness

General and systemic including airway exam

Routine blood investigations Hb10gm CBC 20200cumm RFTs amp

LFTs WNL RBS 320mgdl Serum electrolytes- Sr Na130mEql

Sr K 5mEql Chest Xray increased BVM ECG NSR

Urine routine microscopy

Special investigations Serum and urine ketones ++ ABG- pH725 pO290 pCO228 Sr

bicarbonate15 BE-9 SO297If a classic triad of DKA ie hyperglycemia

ketonemia and metabolic acidosis is seendiagnosis

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

deficiencydependence The presenting symptom for ~ 25

of Type I Diabetics

Stressful precipitating event that results in increased catecholamines cortisol glucagon Infection (pneumonia UTI)Alcohol drugsStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids thiazide diuretics)Non-compliance with insulin

Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation

Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations

respiratory distress Abdominal tenderness (may resemble

acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema

possibly coma

INSULIN Administer short-acting insulin IV (01

unitskg) or IM (03 unitskg) then 01 unitskg per hour by

continuous IV infusion Increase 2- to3-fold if no response by 2ndash

4 h If initial serum potassium is lt 33

meqlcorrect K level while giving insulin to prevent dangerous hypokalemia

Expected fall is 50-100 mgh Transition into SQ when

A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO

FLUID1 Deficit is around 6-8 L ndash need NOT to

replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over

first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash

300mLh Change to 5 glucose and 045 saline

at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)

Watch BP pulse BUNcreatinine and urinary output

Use plasma expandersblood if in shock and does not respond quickly to saline

ELECTROLYTES1 The critical is K2 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+ 1048698 Rehydration rarr uarr urinary secretion of

K+ 1048698 Insulin administration moves K+ from

extracellular to intracellular

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 2: Diabetic ketoacidosis ppt

General and systemic including airway exam

Routine blood investigations Hb10gm CBC 20200cumm RFTs amp

LFTs WNL RBS 320mgdl Serum electrolytes- Sr Na130mEql

Sr K 5mEql Chest Xray increased BVM ECG NSR

Urine routine microscopy

Special investigations Serum and urine ketones ++ ABG- pH725 pO290 pCO228 Sr

bicarbonate15 BE-9 SO297If a classic triad of DKA ie hyperglycemia

ketonemia and metabolic acidosis is seendiagnosis

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

deficiencydependence The presenting symptom for ~ 25

of Type I Diabetics

Stressful precipitating event that results in increased catecholamines cortisol glucagon Infection (pneumonia UTI)Alcohol drugsStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids thiazide diuretics)Non-compliance with insulin

Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation

Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations

respiratory distress Abdominal tenderness (may resemble

acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema

possibly coma

INSULIN Administer short-acting insulin IV (01

unitskg) or IM (03 unitskg) then 01 unitskg per hour by

continuous IV infusion Increase 2- to3-fold if no response by 2ndash

4 h If initial serum potassium is lt 33

meqlcorrect K level while giving insulin to prevent dangerous hypokalemia

Expected fall is 50-100 mgh Transition into SQ when

A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO

FLUID1 Deficit is around 6-8 L ndash need NOT to

replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over

first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash

300mLh Change to 5 glucose and 045 saline

at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)

Watch BP pulse BUNcreatinine and urinary output

Use plasma expandersblood if in shock and does not respond quickly to saline

ELECTROLYTES1 The critical is K2 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+ 1048698 Rehydration rarr uarr urinary secretion of

K+ 1048698 Insulin administration moves K+ from

extracellular to intracellular

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 3: Diabetic ketoacidosis ppt

Special investigations Serum and urine ketones ++ ABG- pH725 pO290 pCO228 Sr

bicarbonate15 BE-9 SO297If a classic triad of DKA ie hyperglycemia

ketonemia and metabolic acidosis is seendiagnosis

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

deficiencydependence The presenting symptom for ~ 25

of Type I Diabetics

Stressful precipitating event that results in increased catecholamines cortisol glucagon Infection (pneumonia UTI)Alcohol drugsStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids thiazide diuretics)Non-compliance with insulin

Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation

Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations

respiratory distress Abdominal tenderness (may resemble

acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema

possibly coma

INSULIN Administer short-acting insulin IV (01

unitskg) or IM (03 unitskg) then 01 unitskg per hour by

continuous IV infusion Increase 2- to3-fold if no response by 2ndash

4 h If initial serum potassium is lt 33

meqlcorrect K level while giving insulin to prevent dangerous hypokalemia

Expected fall is 50-100 mgh Transition into SQ when

A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO

FLUID1 Deficit is around 6-8 L ndash need NOT to

replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over

first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash

300mLh Change to 5 glucose and 045 saline

at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)

Watch BP pulse BUNcreatinine and urinary output

Use plasma expandersblood if in shock and does not respond quickly to saline

ELECTROLYTES1 The critical is K2 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+ 1048698 Rehydration rarr uarr urinary secretion of

K+ 1048698 Insulin administration moves K+ from

extracellular to intracellular

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 4: Diabetic ketoacidosis ppt

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

deficiencydependence The presenting symptom for ~ 25

of Type I Diabetics

Stressful precipitating event that results in increased catecholamines cortisol glucagon Infection (pneumonia UTI)Alcohol drugsStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids thiazide diuretics)Non-compliance with insulin

Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation

Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations

respiratory distress Abdominal tenderness (may resemble

acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema

possibly coma

INSULIN Administer short-acting insulin IV (01

unitskg) or IM (03 unitskg) then 01 unitskg per hour by

continuous IV infusion Increase 2- to3-fold if no response by 2ndash

4 h If initial serum potassium is lt 33

meqlcorrect K level while giving insulin to prevent dangerous hypokalemia

Expected fall is 50-100 mgh Transition into SQ when

A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO

FLUID1 Deficit is around 6-8 L ndash need NOT to

replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over

first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash

300mLh Change to 5 glucose and 045 saline

at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)

Watch BP pulse BUNcreatinine and urinary output

Use plasma expandersblood if in shock and does not respond quickly to saline

ELECTROLYTES1 The critical is K2 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+ 1048698 Rehydration rarr uarr urinary secretion of

K+ 1048698 Insulin administration moves K+ from

extracellular to intracellular

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 5: Diabetic ketoacidosis ppt

Stressful precipitating event that results in increased catecholamines cortisol glucagon Infection (pneumonia UTI)Alcohol drugsStrokeMyocardial InfarctionPancreatitisTraumaMedications (steroids thiazide diuretics)Non-compliance with insulin

Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation

Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations

respiratory distress Abdominal tenderness (may resemble

acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema

possibly coma

INSULIN Administer short-acting insulin IV (01

unitskg) or IM (03 unitskg) then 01 unitskg per hour by

continuous IV infusion Increase 2- to3-fold if no response by 2ndash

4 h If initial serum potassium is lt 33

meqlcorrect K level while giving insulin to prevent dangerous hypokalemia

Expected fall is 50-100 mgh Transition into SQ when

A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO

FLUID1 Deficit is around 6-8 L ndash need NOT to

replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over

first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash

300mLh Change to 5 glucose and 045 saline

at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)

Watch BP pulse BUNcreatinine and urinary output

Use plasma expandersblood if in shock and does not respond quickly to saline

ELECTROLYTES1 The critical is K2 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+ 1048698 Rehydration rarr uarr urinary secretion of

K+ 1048698 Insulin administration moves K+ from

extracellular to intracellular

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 6: Diabetic ketoacidosis ppt

Polyuria Polydypsia Blurred vision NauseaVomiting Abdominal Pain Fatigue Confusion Obtundation

Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations

respiratory distress Abdominal tenderness (may resemble

acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema

possibly coma

INSULIN Administer short-acting insulin IV (01

unitskg) or IM (03 unitskg) then 01 unitskg per hour by

continuous IV infusion Increase 2- to3-fold if no response by 2ndash

4 h If initial serum potassium is lt 33

meqlcorrect K level while giving insulin to prevent dangerous hypokalemia

Expected fall is 50-100 mgh Transition into SQ when

A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO

FLUID1 Deficit is around 6-8 L ndash need NOT to

replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over

first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash

300mLh Change to 5 glucose and 045 saline

at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)

Watch BP pulse BUNcreatinine and urinary output

Use plasma expandersblood if in shock and does not respond quickly to saline

ELECTROLYTES1 The critical is K2 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+ 1048698 Rehydration rarr uarr urinary secretion of

K+ 1048698 Insulin administration moves K+ from

extracellular to intracellular

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 7: Diabetic ketoacidosis ppt

Tachycardia Dehydration hypotension Tachypnea Kussmaul respirations

respiratory distress Abdominal tenderness (may resemble

acute pancreatitis or surgical abdomen) Lethargy obtundation cerebral edema

possibly coma

INSULIN Administer short-acting insulin IV (01

unitskg) or IM (03 unitskg) then 01 unitskg per hour by

continuous IV infusion Increase 2- to3-fold if no response by 2ndash

4 h If initial serum potassium is lt 33

meqlcorrect K level while giving insulin to prevent dangerous hypokalemia

Expected fall is 50-100 mgh Transition into SQ when

A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO

FLUID1 Deficit is around 6-8 L ndash need NOT to

replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over

first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash

300mLh Change to 5 glucose and 045 saline

at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)

Watch BP pulse BUNcreatinine and urinary output

Use plasma expandersblood if in shock and does not respond quickly to saline

ELECTROLYTES1 The critical is K2 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+ 1048698 Rehydration rarr uarr urinary secretion of

K+ 1048698 Insulin administration moves K+ from

extracellular to intracellular

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 8: Diabetic ketoacidosis ppt

INSULIN Administer short-acting insulin IV (01

unitskg) or IM (03 unitskg) then 01 unitskg per hour by

continuous IV infusion Increase 2- to3-fold if no response by 2ndash

4 h If initial serum potassium is lt 33

meqlcorrect K level while giving insulin to prevent dangerous hypokalemia

Expected fall is 50-100 mgh Transition into SQ when

A Plasma glucose is less than 250 mgdlB DKA has resolved (usually less than 12 hs)C Patient is tolerating PO

FLUID1 Deficit is around 6-8 L ndash need NOT to

replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over

first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash

300mLh Change to 5 glucose and 045 saline

at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)

Watch BP pulse BUNcreatinine and urinary output

Use plasma expandersblood if in shock and does not respond quickly to saline

ELECTROLYTES1 The critical is K2 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+ 1048698 Rehydration rarr uarr urinary secretion of

K+ 1048698 Insulin administration moves K+ from

extracellular to intracellular

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 9: Diabetic ketoacidosis ppt

FLUID1 Deficit is around 6-8 L ndash need NOT to

replace all of it with IV fluid Replace fluids 2ndash3 L of 09 saline over

first 1ndash3 h (10ndash15 mLkg per hour) Subsequently 045 saline at 150ndash

300mLh Change to 5 glucose and 045 saline

at 100ndash200 mLh when plasma glucose reaches 250 mgdL (14 mmolL)

Watch BP pulse BUNcreatinine and urinary output

Use plasma expandersblood if in shock and does not respond quickly to saline

ELECTROLYTES1 The critical is K2 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+ 1048698 Rehydration rarr uarr urinary secretion of

K+ 1048698 Insulin administration moves K+ from

extracellular to intracellular

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 10: Diabetic ketoacidosis ppt

ELECTROLYTES1 The critical is K2 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+ 1048698 Rehydration rarr uarr urinary secretion of

K+ 1048698 Insulin administration moves K+ from

extracellular to intracellular

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 11: Diabetic ketoacidosis ppt

Replace K+ 10 meqh when

plasma K+ lt 55 meqL ECG normal urine flow and normal Cr

40ndash80 meqh when plasma K+ lt 35 meqL or if bicarbonate is given

SERUM K Rate hour LOW (lt35) 40 Meq

Normal (35-50) 20 Meq Normal pH lt70 or

EKG changes 40 Meq

High (gt50) Hold until level normal

High (gt50) pH lt 70 or EKG changes

10-20 meq

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 12: Diabetic ketoacidosis ppt

BICARBONATE1 Usually NOT necessary2 It may even be dangerous and

precipitate hypokalemia cerebral acidosis and cardiac dysfunction

3 For very severe acidosis (pH lt69) use very small amounts enough to elevate pH to 70

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 13: Diabetic ketoacidosis ppt

PHOSPHATE AND OTHER ISSUES

Supplementation only advised if Serum phosphate conc lt10mgdl or in the presence of anemia cardiac dysfunction

If needed 20-30 mEql potassium phosphate can be given

Broad spectrum antibiotic coverage is required

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 14: Diabetic ketoacidosis ppt

Measure capillary glucose every 1ndash2 h electrolytes (especially K+ bicarbonate phosphate)

amp anion gap every 4 h for first 24 h Monitor BP pulse respirations mental status fluid

intake and output every 1ndash4 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 150ndash250 mgdL and acidosis is resolved Insulin infusion may be decreased to 005ndash01

unitskghr

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 15: Diabetic ketoacidosis ppt

Cerebral edema First 24hrs Mental status changes Tx Mannitol May require intubation

with hyperventilation Shock

If not improving with fluids ro MI

Vascular thrombosis Severe dehydration Cerebral vessels Occurs hours to days

after DKA

Pulmonary Edema and Hypoxemia

Iatrogenic hypoglycemia and hypokalemia

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 16: Diabetic ketoacidosis ppt

With a central line already in situ patient is taken inside the OT after checking starvation and high risk consent

Adequate amount of crossmatched blood is kept ready

The standard monitors attached HGTCVP and urine output monitoring is essential

IV fluid is attached

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 17: Diabetic ketoacidosis ppt

Low dose unilateral sub arachnoid block can be given using 05(H) InjBupivacaine and Inj Fentanyl as additive making a total volume of 12-14cc

Excellent analgesiano need to use NSAIDS or opiods intra op

Hypoglycemia amp hyperglycemic coma can be detected early

Avoidance of ETT amp resultant infection

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 18: Diabetic ketoacidosis ppt

Disadvantages Inadvertant higher level of block can

result in hypotension complicated by autonomic neuropathy in DM

Sympathetic blockade can impair control of insulin secretion

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 19: Diabetic ketoacidosis ppt

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

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 20: Diabetic ketoacidosis ppt

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

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 21: Diabetic ketoacidosis ppt

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

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 22: Diabetic ketoacidosis ppt

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 ico hyperkalemia

After induction Injmidazolam and opiod(preferably fentanyl) is given in titrated doses for analgesia and sedation

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes

Page 23: Diabetic ketoacidosis ppt

Maintenance oxygen amp nitrous oxide and sevoflurane or Isoflurane

Reversalroutine reversal Extubation after adequate recovery of

airway reflexes Post op monitoring blood sugar

levelserum and urine ketones serum electrolytes