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Shock in Obstetrics

Chapter · January 2020


DOI: 10.1007/978-981-10-4953-8_54

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Rajesh Kumar Verma Rohini Rao


Indira Gandhi Medical College Indira Gandhi Medical College and Research Institute
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1 Shock in Obstetrics
54
2 Rajesh Kumar Verma, Rohini Rao,
3 and Kunal Kumar Sharma

4 SHOCK—defined as failure of circulation which ( b) Concealed intrauterine haemorrhage. 23


5 is life threatening. It is characterised by low per- (c) Forceps delivery or breech delivery in incom- 24
6 fusion of vital organs due to low cardiac output. pletely dilated cervix. 25
(d) During internal version of foetus. 26
7 Types (e) Crédé’s method. 27
8 1. Hypovolaemic—due to body fluid or blood (f) Uterine rupture. 28
9 loss (g) Uterine inversion. 29
10 2. Cardiogenic—direct damage to the heart (h) Splanchnic shock—Seen due to accumula- 30
11 3.
Extracardiac obstructive—obstruction to tion of blood in splanchnic area after sud- 31
12 blood flow den emptying of the uterine cavity, e.g. 32
13 4. Distributive—abnormal distribution of blood rupture of membranes in a patient of 33
14 flow polyhydramnios. 34

15 Shock in Obstetrics Cardiogenic shock: It is observed in condi- 35


tions in which cardiac myocytes are unable to 36
16 Haemorrhagic shock (most common): generate adequate stroke volume due to lack of 37
17 (a) Haemorrhage in antenatal period during the efficient contraction, myocardial infarction and 38
18 first trimester cardiac failure. 39
19 (b) Antepartum haemorrhage Endotoxic shock: It occurs due to toxins that 40
20 (c) Postpartum haemorrhage precipitate vascular disturbance. 41
Anaphylactic shock: It is seen in hypersensi- 42
tivity reactions to drugs. 43
21 Neurogenic shock:
22 (a) Ruptured ectopic pregnancy. Other causes: 44
(a) Embolism: amniotic fluid, air or thrombus 45
R. K. Verma (*) (b) Mendelson’s syndrome 46
Department of Anaesthesia, IGMC,
Shimla, Himachal Pradesh, India Note: A patient can present with shock due to 47
R. Rao multifactorial aetiologies, e.g. incomplete abor- 48
Department of Obstetrics & Gynecology, IGMC, tion leading to haemorrhagic and endotoxic 49
Shimla, Himachal Pradesh, India
shock, whereas ruptured ectopic and uterine rup- 50
K. K. Sharma ture eventually lead to haemorrhagic and neuro- 51
Civil Hospital Sunni,
Shimla, Himachal Pradesh, India genic shock. 52

© Springer Nature Singapore Pte Ltd. 2019 537


A. Sharma (ed.), Labour Room Emergencies, https://doi.org/10.1007/978-981-10-4953-8_54
538 R. K. Verma et al.

53 Haemorrhagic shock in obstetrics is due to Estimation of blood: 75


54 antepartum or postpartum haemorrhage. Fully soaked 4″ × 4″ sponge contains approxi- 76
55 Haemorrhagic shock is classified as in Table 54.1: mately 10 mL of blood. 77
56 A more detailed parameter-based ATLS clas- Soaked laparotomy pads contain 100–150 mL 78
57 sification of shock is depicted in Table 54.2: of blood. 79
58 Measurement of surgical blood loss: Measurement of blood in suction canister 80
59 Anaesthesiologists and obstetricians frequently after evacuation of amniotic fluid/dilutional 81
60 underestimate blood loss. Massive blood loss saline (Fig. 54.1). 82
61 leads to errors in judgement of estimation, which Laboratory evaluation: 83
62 is responsible for inadequate replacement of Serial haemoglobin/haematocrit measure- 84
63 intravascular volume. The young patients exhibit ments—It basically reflects ratio of blood loss to 85
64 signs of hypotension and tachycardia after sig- plasma. Used for cases where the operative pro- 86
65 nificant haemorrhage has already taken place. cedure is for long duration. 87
66 Haemodynamic management requires continu- Gravimetric method: 88
67 ous assessment of patient status by clinical Blood loss is estimated by gain in weight of 89
68 assessment, by classical monitoring equipment swabs and towels after soakage with blood. 90
69 and by microprocessor-enabled monitors like
70 Flotrac Vigileo™. The blood loss measurement
71 can be done by the following methods:
72 Visual assessment:
73 Direct measurement of blood collected in cali-
74 brated drapes.

t1.1 Table 54.1  Categories of shock


t1.2 Whole
t1.3 blood
t1.4 volume
t1.5 Category loss % Pathophysiology
t1.6 Mild <20% Peripheral
t1.7 (compensated) vasoconstriction to
t1.8 preserve cerebral and
t1.9 coronary blood flow
t1.10 Moderate 20–40% Decreased perfusion of
t1.11 kidneys, intestine and
t1.12 pancreas
t1.13 Severe >40% Decreased coronary
t1.14 (uncompensated) and cerebral perfusion Fig. 54.1  Disposable calibrated drape

Table 54.2  Advanced trauma life support (ATLS) classification of shock t2.1

Class 1 Class 2 Class 3 Class 4 t2.2


Blood loss (%) <15 15–30 30–40 >40 t2.3
Heart rate (beats/min) <100 >100 >120 >140 t2.4
Systolic blood pressure Normal Normal Decreased Decreased t2.5
(mmHg) t2.6
Pulse pressure Normal or Decreased Decreased Decreased t2.7
increased t2.8
Respiratory rate (breaths/min) 14–20 20–30 30–40 >35 t2.9
Mental state Slightly anxious Mildly Anxious, Confused, t2.10
anxious confused lethargic t2.11
54  Shock in Obstetrics 539

91 However, it underestimates blood loss by 25% reflect the changes in blood volume intraopera- 113
92 because it doesn’t take into account the blood tively (Table 54.3). 114
93 loss by evaporation, blood lost in crevices of floor Transfusion trigger is the haemoglobin level 115
94 and blood collected in body cavities. Whereas, below which transfusion of RBCs is indicated. 116
95 overestimation can also occur if the swabs also Various guidelines are as follows: 117
96 get soaked with pus, urine and irrigational Habibi recommendations—Transfuse blood if: 118
97 fluids.
98 Colorimetric method: • Hb ≤ 8 g/dL in all types of patients 119
99 Swabs, sponges and towels are mixed thor- • Hb  ≤  10  g/dL in patient of ischaemic heart 120
100 oughly with known volume of fluid. The change disease, emphysema 121
101 in optical density of water is measured at the isos- • Hb ≤ 10 g/dL with autologous blood 122
102 bestic absorption wavelength of haemoglobin. • Hb ≤ 12 g/dL in ventilator-dependent patient 123
103 Radioactive tracer dilution method [1]: Either
104 patient’s RBCs are labelled with Cr51 or pooled If blood loss >20% blood volume in adults or 124
105 human albumin labelled with I125 is used. The ≤100 mL in paediatric patients 125
106 activity of tracer is first measured and then Herbert recommendations—Transfuse blood 126
107 injected intravenously. The activity remaining in if: 127
108 the syringe is measured and it is deducted from
109 the amount of isotope injected. After 15  min, • Hb ≤ 10 g/dL in unstable angina and anterior 128
110 sample is drawn from opposite arm, and its activ- wall MI 129
111 ity is measured to estimate the change in blood • Hb levels between 10 and 12 g/dL in critically 130
112 volume. Repeated measurements over time ill patients 131

Colorimeter reading  volume of solution


Blood loss 
200  patient 's Hb  g / dL 

ASA 1996 guidelines: complications of inadequate oxygenation and


Transfusion of blood just based on Hb levels cardiovascular status.
without considering other conditions is not indi- The American College of Surgeons Trauma
cated. Whenever possible, use acute normovolae- Committee’s Advanced Trauma Life Support
mic haemodilution, preoperative autologous (ATLS) system classifies hypovolaemic shock
blood donation and post-op modifications to into four stages based on the volume of haemor-
reduce blood loss. Transfusion is RARELY rhage. Obstetric patients are often mildly tachy-
required if Hb is >10 g/dL, whereas it is ALWAYS cardiac. However, tachycardia of more than 120
required if Hb is <6  g/dL.  If Hb is between 6 beats per minute is exhibited when the patient has
and 10 g/dL, the blood transfusion depends on had a blood loss amounting to 30–40% of her

Table 54.3  American College of Surgeons Advanced Trauma Life Support Classification of Haemorrhage Severity t3.1

Haemorrhage severity Class 1 Class 2 Class 3 Class 4 t3.2


Blood loss (mL) < 750 750–1500 1500–2000 >2000 t3.3
Pulse rate (per minute) <100 >100 >120 >140 t3.4
Blood pressure Normal Normal Decreased Decreased t3.5
Pulse pressure (mmHg) Normal Decreased Decreased Decreased t3.6
Respiratory rate (per minute) 14–20 20–30 30–40 >40 t3.7
Urine output (mL/h) >30 20–30 5–15 Negligible t3.8
Central nervous system (mental status) Slightly anxious Mildly anxious Anxious confused Lethargic t3.9
540 R. K. Verma et al.

t4.1 Table 54.4  Trigger thresholds for MEOWS parameters The haemoglobin concentration determines the 162
t4.2 Yellow oxygen content in the blood and also the oxygen 163
t4.3 Red trigger trigger delivery to the tissues. However, compensatory 164
t4.4 Temperature (oC) <35 or >38 35–36 physiologic responses offset the negative effect of 165
t4.5 Systolic blood <90 or >160 150–160 or
anaemia on oxygen transport. There occurs an 166
t4.6 pressure (mmHg) 90–100
t4.7 Diastolic blood >100 90–100 increase in cardiac output by combined effect of 167
t4.8 pressure (mmHg) tachycardia and raised stroke volume. The blood 168
t4.9 Respiratory rate <10 or >30 21–30 viscosity and systemic vascular resistance 169
t4.10 (breaths/min) decrease, thereby augmenting blood flow to tis- 170
t4.11 Oxygen saturation <95 – sues. Also, there occurs an increase in tissue oxy- 171
t4.12 (%)
gen extraction. As haemoglobin concentration 172
t4.13 Pain scorea – 2–3
t4.14 Neurologic response Unresponsive, Voice
falls to 5  g/dL, the systemic vascular resistance 173
t4.15 pain decreases, whereas the heart rate, stroke volume 174
t4.16 a
Pain score: 0 = no pain at rest or movement; 1 = no pain and cardiac index increase. The rate of oxygen 175
t4.17 at rest, slight pain on movement; 2 = intermittent pain at transport and mixed venous oxyhaemoglobin satu- 176
t4.18 rest, moderate pain on movement; 3  =  moderate pain at ration decrease at a haemoglobin level of 5.0 g/dL. 177
t4.19 rest, severe pain on movement
Risks of blood transfusion include haemolytic 178
reactions, transfusion-associated circulatory 179
132 total blood volume. Change in blood pressure overload (TACO), transfusion-related acute lung 180
133 and neurological status occurs later. injury (TRALI), transfusion-related immuno- 181
134 The modified early obstetric warning system modulation (TRIM) and bacterial and viral 182
135 (MEOWS) was established in the backdrop of infections. 183
136 this knowledge, with the primary aim to detect
137 impending adverse events in a patient of shock.
138 MEOWS is not specific to haemorrhage, but it 54.1 Management 184
139 has a positive predictive value of 39% and a nega- of Haemorrhagic Shock 185
140 tive predictive value of 98% in predicting mater- in Obstetric Patient 186
141 nal morbidity [2] (Table 54.4).
142 The rate of development of coagulopathy in # 1 Patient preparation: 187
143 obstetric haemorrhage is another major concern.
144 The pathophysiology involves rapid consumption • Two large-bore 14–16 G IV canula 188
145 of coagulation factors, like fibrinogen. Postpartum • Oxygen at 6–8 L/min via facemask 189
146 haemorrhage and placental abruption trigger • CVP and IBP access 190
147 coagulopathy which is not in proportion to the • Foley’s catheterization 191
148 amount of haemorrhage that has occurred in the • Correct hypovolemia by crystalloids or 192
149 patient. Once coagulopathy develops, the require- colloids 193
150 ment for additional resources like blood products • Arrange blood 194
151 increases; therefore, the institutional protocol in • Correct coagulopathy by FFP, cryoprecipitate, 195
152 such a situation must be clearly defined in platelet concentrate, NovoSeven 196
153 advance in order to mobilize personnel and • Emergency coagulation profiling of the patient 197
154 resources. Team practice drills of using this pro- • Anti-aspiration prophylaxis 198
155 tocol have shown to decrease the severity of
156 haemorrhage and mortality. #2 Control the bleeding: 199
157 The AABB recommends limited use of trans- Surgical management 200
158 fusion after moderate haemorrhage in a haemo-
159 dynamically stable adult patient. This advice • Uterine tamponade by Sengstaken-Blakemore 201
160 takes into account the risks of anaemia while catheter or bimanual compression 202
161 comparing it with the risks of transfusion. • B-Lynch compression sutures 203
54  Shock in Obstetrics 541

204 • Radiological embolization with gelatin sponge, administration is not recommended due to high 251
205 polyurethane foam or polyvinyl methyl alco- incidence of nausea and vomiting. The duration 252
206 hol particle of uterotonic effect is 2–4 h. Due to the produc- 253
207 • Arterial ligation of uterine artery, ovarian tion of tetanic uterine contractions, the use of 254
208 artery or internal iliac artery methylergonovine is restricted in postpartum 255
209 • Emergency hysterectomy if above measures fail period. Side effects of this drug include hyperten- 256
sion, coronary vasospasm, myocardial ischaemia 257
210 Anaesthetic management: General anaes- and seizures. 258
211 thesia is preferred for patient with uncontrolled Carboprost [15-methyl prostaglandin F2α]: It 259
212 haemorrhage, coagulopathy and foetal distress. is a synthetic prostaglandin analogue which is 260
213 Rapid sequence induction of anaesthesia with given in a dose of 0.25 mg (250 μg) intramuscu- 261
214 ketamine or etomidate using smaller-sized larly. This dose can be repeated every 15–30 min 262
215 endotracheal tube is advocated. Maintenance to a maximum cumulative dose of 2 mg. Its effi- 263
216 of anaesthesia with TIVA technique using ket- cacy in reducing postpartum haemorrhage is well 264
217 amine and propofol achieves optimal results in documented. Adverse effects associated with its 265
218 patients with uncontrolled bleeding. Once use are bronchospasm, dyspnoea and hypoxae- 266
219 bleeding gets controlled, balanced anaesthesia mia. These are seen in patients with coexisting 267
220 technique using volatile agents can be started. disease like asthma. It is also not advocated to 268
221 FiO2 is kept at 100% initially, thereafter as per use it in patients with acute PID, cardiac disease 269
222 the maternal tolerance; nitrous oxide or isoflu- and renal disease. 270
223 rane 0.5% is started. Pancuronium is preferred Misoprostol [prostaglandin E1 analogue]: 271
224 for patient with obstetric haemorrhage in The usual dose to treat patients presenting with 272
225 shock. Cisatracurium is preferred over atracu- postpartum haemorrhage is 600–1000 μg per rec- 273
226 rium, especially if the patient has shock associ- tum. Other routes are oral, buccal, vaginal and 274
227 ated with acute renal failure. Vecuronium is sublingual. This drug belongs to FDA category X 275
228 preferred in uncomplicated case presenting for pregnant patients. Adverse effects like fever, 276
229 only with massive blood loss. Fentanyl chills, nausea, vomiting and diarrhoea can occur 277
230 5–10  μg/kg provides adequate analgesia to with its usage. 278
231 such patients. In order to provide uterine relax- Intramyometrial PGE2 0.5  mg or PGF2α 279
232 ation during dilatation and curettage, use of 0.2 mg 280
233 volatile anaesthetic agents or intravenous Medical management [3] 281
234 nitroglycerin is advocated.
235 Uterotonic therapy is given by the following • If Hb <9g/dL, start RBC transfusion until Hb 282
236 drugs: levels increase more than 9 g/dL. 283
237 Oxytocin: The convention of administering • Identify and correct platelet or coagulation 284
238 10–40 IU infused in 1000 mL crystalloid solution abnormalities using Sonoclot or 285
239 at an unspecified rate can lead to catastrophic thromboelastogram. 286
240 scenarios in these patients presenting with hypo- • Measure CVP and keep its target goal to be 287
241 volaemic haemorrhagic shock. Phenylephrine is >8 mmHg. 288
242 a selective α1 agonist, which when given in inter- • Also keep MAP >65 mmHg. 289
243 mittent boluses of 25–50  mg mitigates the hae- • If MAP <65 mmHg but CVP >8 mmHg, start 290
244 modynamic effects of oxytocin. The initial rate of vasopressors like noradrenaline or dopamine. 291
245 oxytocin infusion is recommended to be 0.3 IU/ • If CVP <8 mmHg, give fluid boluses with 0.9 292
246 min (i.e. ED90). In case of inadequate response, NaCl or RL at 20 mL/kg. 293
247 the infusion rate should be increased to 0.6  IU/ • Alternatively noninvasive cardiac output mon- 294
248 min (i.e. twice the ED90 value). itoring devices like Flotrac shall help to deter- 295
249 Methylergonovine: The recommended dose mine whether the patient shall respond to iv 296
250 is 0.2  mg intramuscular. Bolus intravenous fluids or to vasopressor support. 297
542 R. K. Verma et al.

298 • Tranexamic acid 1 g iv bolus over 5 min can • If mean arterial pressure is <60 mmHg, start 338
299 be repeated after 30–60 min only once. vasopressors in the following dosages: 339
300 • FFP: PRBC transfusion in the ratio 1:1.4 –– Noradrenaline at 0.05–0.5 μg/kg/min 340
301 • Platelet transfusion if platelet count is –– Dopamine at 5–20 μg/kg/min 341
302 <50,000/mm [3] –– Adrenaline at 0.05–2 μg/kg/min 342
303 • NovoSeven 60–120 μg/kg iv [4] –– Phenylephrine at 2–10 μg/kg/min 343
–– Vasopressin at 0.04 units/min 344
304 Other measures • Once the mean arterial pressure becomes 345
more than 60  mmHg, measure the central 346
305 • Prevention of hypothermia venous blood oxygen saturation (ScvO2). 347
306 • Rewarming of fluids administered • If ScvO2 is <70%, look at haematocrit. If hae- 348
307 • Cell salvaging devices matocrit is <30, transfuse PRBCs. 349
308 • Corticosteroids to tide over the stress response • If cardiac index is <3.5 L/min/m2, start dobu- 350
309 • Meticulous correction of arterial blood gas tamine at 2.5–10 μg/kg/min. 351
310 parameters • Once ScvO2 is >70% but vasopressors are still 352
required, look at the APACHE II score of the 353
311 Septic shock in obstetric patient patient. If it is ≥25, administer activated 354
312 The mortality associated with this type of shock Drotrecogin alfa. 355
313 ranges from 30 to 50%. Due to the predominant • But if patient is in moribund state and with 356
314 rural population in India, many cases of gynaeco- increased risk of bleeding, measure serum 357
315 logical infections are underdiagnosed at periph- cortisol level. 358
316 eral institutes. Also the practice by quacks at the • If serum cortisol is <15 μg/mL, you can con- 359
317 remote villages under lack of sterile equipment sider corticosteroid replacement therapy. 360
318 predisposes a large number of females for septic However, this therapy is unlikely to benefit if 361
319 shock. The underlying pathophysiology in sepsis serum cortisol is more than 34 μg/mL. 362
320 consists of a matrix of events that are associated • Initial empirical antibiotic management is 363
321 with immune system and coagulation system. based on the likely clinical presentation of 364
the patient. Usually we start with a broad-­365
spectrum antibiotic that covers most types 366
322 54.2 Management [5, 6] of bacteria [7]. Other factors to be consid- 367
ered are the healthcare-associated infections 368
323 The patient presents with end-organ dysfunction and the community prevalent infections in 369
324 along with systolic blood pressure less than the area. Once culture reports are available, 370
325 90  mmHg, mean arterial pressure less than the organism-­ based antibiotic regimen is 371
326 60  mmHg and blood lactate levels more than started. 372
327 4 mmol/L. • The sooner the management of the patients 373
starts, the more likely is their survival. 374
328 • Resuscitate the patient with crystalloids at
329 20 mL/kg.
330 • If systolic blood pressure is still less than References 375
331 90  mmHg and mean arterial pressure is still
332 less than 60  mmHg, insert a CVP line for 1. Bassingthwaighte JB, Holloway GA.  Estimation of 376
333 guidance of fluid management. blood flow with radioactive tracers. Semin Nucl Med. 377
334 • If CVP is <8 mmHg, repeat the fluid bolus of 1976;6(2):141–61. 378
2. Singh S, McGlennan A, England A, Simons R.  A 379
335 crystalloids at 20  mL/kg. Once the CVP is validation study of the CEMACH recommended 380
336 ≥8  mmHg, measure the mean arterial modified early obstetric warning system (MEOWS). 381
337 pressure. Anaesthesia. 2012;67:12–8. 382
54  Shock in Obstetrics 543

383 3. Nunez TC, Cotton BA. Transfusion therapy in haem- 6. Rivers E, Nguyen B, Havstad S. Early goal-directed 391
384 orrhagic shock. Curr Opin Crit Care. 2009;15:536–41. therapy in the treatment of severe sepsis and septic 392
385 4. Stein DM, Dutton RP. Use of recombinant factor VII shock. N Engl J Med. 2001;345:1368–77. 393
386 a in trauma. Curr Opin Crit Care. 2009;15:536–41. 7. Micek ST, Welch EC, Khan J.  Empiric combination 394
387 5. Dellinger RP, Levy MM, Carlet JM, et al. Surviving antibiotic therapy is associated with improved out- 395
388 Sepsis Campaign: international guidelines for man- come against sepsis due to Gram-negative bacteria : a 396
389 agement of severe sepsis and septic shock: 2008. Crit retrospective analysis. Antimicrob Agents Chemother. 397
390 Care Med. 2008;36:296–327. 2010;54:1742–8. 398
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