LECTURE 7 : SHOCK IN ADULT IGAG Utara Hartawan
OBJECTIVE 1. To understand the definition, type and pathophysiology of shock
2. Implement a general strategy in the patients approach to shock through symptoms,
physical examination and special technique examination.
3. Able to perform assessment, differential diagnosis, provide early treatment and refer
patients with shock
4. Knowing the patients prognosis with shock INTRODUCTION
Shock is a clinical expression of circulatory failure that results in inadequate cellular oxygen utilization. Shock is a common condition that often occurs in critical conditions,
which occurs in more than one-third of patients treated in intensive care. The diagnosis of shock can be established based on clinical, haemodynamic and biochemical criteria, which
can generally appear in 3 forms. The first is arterial hypotension, but the magnitude of hypotension can vary widely, especially in patients with chronic hypertension. Typically, in
adults, the systolic arterial pressure is less than 90 mmHg or an average arterial pressure less than 70 mmHg, with tachycardia. Secondly, there is a clinical sign of tissue hypoperfusion,
seen through the three Windows of the body: skin cold and moist skin, with vasoconstriction and cyanosis, kidney urine output 0.5 ml per kilogram body weight per
hour, and neurologic changed mental state, which usually includes obtundation, disorientation, and confusion. Third, accompanied by conditions of hyperlactatemia, which
indicate abnormal cellular oxygen metabolism 1.5 mmol per liter. Shocks are classified as: hypovolemic, cardiogenic, obstructive and distributive.
PATHOPHYSIOLOGY
Shock may originate from four conditions of pathophysiological mechanisms: hypovolemia from internal or external fluid loss, cardiogenic factors eg, acute myocardial
infarction, end-stage cardiomyopathy, advanced heart valve disease, myocarditis, or cardiac arrhythmias, obstructive eg embolism Lung, cardiac tamponade, or tension pneumothorax,
and distributive factors such as severe sepsis or anaphylaxis with the release of inflammatory mediators. The first three mechanisms are characterized by low cardiac output
and, therefore, inadequate oxygen transport. In distributive shocks, the major deficits are located on the peripheral, accompanied by decreased systemic vascular resistance and
oxygen extraction disorders. Usually, in such cases cardiac output increases, although it may be low due to associated myocardial depression. Patients with acute circulatory failure often
have this combination. For example, patients with distributive shock from severe pancreatitis, anaphylaxis, or sepsis also experience hypovolemia and cardiogenic shock in
the form of myocardial depression.
The three main factors that determine the delivery of oxygen to the tissues are
cardiac output, defined as the stroke volume of heart rate; oxygen saturation bound to Hgb O2 X100 capacity and the amount of dissolved oxygen in the blood, defined as O2
content mldl blood = Hgb x 1.39 X sat O2 + 0.003 x PaO2.
Any or all of these factors may be disrupted resulting in a decrease in the release of oxygen to tissue levels in the vital organs. The result of a disturbance in these vital organs is
Medical Education Unit Faculty of Medicine Udayana University
38
called shock. Shock begins with a simple state, to the very severe state of the imbalance between the supply and the need for oxygen.
Hypovolaemia leads to increased activity of baroreceptor of the aortic arch and carotid. There is also an increase in baroreceptor activity in the right atrium. The activity of
the sympathetic nervous system increases and results in stimulation of the heart and peripheral vasoconstriction. The pituitary gland releases ACTH and ADH, resulting in
increased cortisol levels in the blood and sodium and water retention. Increased adreno- cortical activity was soon followed by epinephrine and norepinephrine release. Increased
plasma renin-angiotensin-aldosterone results in greater water and sodium retention and peripheral vasoconstriction occurs more severely. As the hypovolemia weighs up, the
compensation mechanism becomes lost and the organ functional disorder becomes more severe.
In addition, the vasoactive hormone is released during shock syndrome, such as prostaglandin, histamine, bradykinin, serotonin, β-endorphin, MDF myocardial depressant
factor and cachectin. All of these substances will affect the perfusion of internal organs and may increase the permeability of blood vessels and myocardium and platelet function.
SYMPTOMPS
Hypotension and vasoconstriction appear in hemorrhagic shock, hypovolemic shock and cardiogenic shock due to decreased perfusion and abnormalities of vital organs. Where
there is a change of the regional vascular resistance thereby reducing the perfusion pressure, thus perfusion to the vital organs can be maintained. In general, the skin becomes cold, moist
and wrinkled. Superficial veins will collapse. Brain circulation is also disrupted as well as skin and other organs, which can lead to classic symptoms of confusion and disorientation.
Cerebral perfusion pressure is the difference between mean arterial pressure and intracranial pressure or right atrial pressure, which is higher CPP = MAP - ICP. Brain auto regulation is
still good at mean arterial pressure between 50 mmHg and 150 mmHg with a rightward shift in chronic hypertension. In hypotension that accompanies shock occurs mental status
changes ranging from agitation, anxiety accompanied by feelings of hovering, then going into a coma. This occurs due to the decrease of cerebral perfusion below the critical value.
Of course the patients response will be clear and appropriate after resuscitation action to improve the hemodynamic state in shock.
Table 1. Early symptoms on shock Organ System
Clinical signs symptoms Cause
CNS Decrease of conciousness
Decrease in CPP CVS
Tachycardia The Adrenergic Stimulus
Dysrhythmias Ischemic Coronary
Hypotension Decreased
contractility, MDF ischaemia, or RVF,
also decreased SVR or preload
Murmurs Valvular dysfunction
JVP increase decrease Decrease in volume
preload or RV failure Respiration
Takipneu Pulmonary
edema,
Medical Education Unit Faculty of Medicine Udayana University
39
respiratory muscle failure, sepsis, acidosis, hypoxemia
Renal Oliguria
Decreased perfusion,
constriction of afferent arterioles
Skin Cold, pale, sweat
Vasoconstriction, sympathetic stimulation
Other Lactic acidosis
Anaerobic metabolism Fever
Infection of hepatic dysfunction
CNS=central nervous system; CVS=cardiovascular system; CPP=cerebral perfusion pressure; MDF=myocardial depressant factor; RVF=right ventricular failure;
SVR=systemic vascular resistance.
The state of shock will affect the heart. Coronary perfusion pressure pressure difference between diastolic pressure and left ventricular diastolic end pressure will
decrease due to hypotension and shock. Tachycardia or bradycardia reflex will also decrease diastolic filling of the coronary arteries. A decrease in mean arterial pressure is an important
sign due to decreased systolic blood pressure; Peripheral vascular pressure increases and cardiac output decreases.
In septic shock where cardiac output increases and systemic vascular resistance decreases, heat, seizures and blood cell count are often elevated in this state. The pulse
becomes fast and not palpable. Increased left ventricular diastolic end pressure may result in pulmonary edema and respiratory failure that may occur along with hypoxemia. If diastolic
pressure decreases, coupled with increased LVEDP left ventricle end-diastolic pressure indicates coronary hypo perfusion and myocardial ischemia. Diastolic blood pressure is
directly related to arterial vasoconstriction, whereas pulse systolic-diastolic is associated with large stroke volume and number of aortic branches and aortic stiffness. Systolic blood
pressure reflects all combinations of these factors. In cardiogenic shock that may be due to chronic heart failure CHF, shortness, tachypnea, pulmonary edema with a decrease in PaO2
and the sound gallop or the third heart sounds S3 gallop.
The renal auto regulation system is also maintained, but with decreased perfusion due to hypotension, decreased glomerular filtration, which is clinically known as oliguria 25-
30 ml hr 70 kg. In this situation there will be redistribution of cortical renal blood flow to the medulla and urine becomes more concentrated. Sodium urine decreased 10 mEq L.
The presence of oliguria is one sign of shock, and urine repair is an important key in successful resuscitation in shock patients. Sometimes a lot of urine production occurs in
renal failure and is confusing at the start of the diagnosis, especially in kidneys with normal or increased urine production.
Integumentary systems are also affected by decreased perfusion and vasoconstriction reflected from cold skin, changing from pale to grayish to cyanosis. The activity of the
sympathetic nervous system results in increased production of sweat a cholinergic sympathetic response.
Metabolic acidosis almost always accompanies shock with the accumulation of lactic acid into hypoxemia. Anaerobic metabolism as a complication due to decreased liver
function that can produce lactic acid.
Medical Education Unit Faculty of Medicine Udayana University
40
Thus, shock indicates a perfusion disorder characterized by decreased cardiac output or distribution disturbance. It may also be the inability of the tissue to utilize a substrate,
thereby resembling a state of hypo perfusion. Blood flow to various organs is seen from the relationship between perfusion pressure and blood vessel resistance in these organs. In
shock, this relationship is influenced by many factors.
PRIORITY AND TARGET THERAPY
In general, there are four phases in shock treatment. Target therapy and monitoring need to be adapted to each phase. In the first phase salvage, the goal of therapy is to
achieve minimum blood pressure and adequate cardiac output for minimal survival. Close monitoring is required; in many cases, invasive monitoring can also be used in arterial and
central venous catheters. Lifesaving procedures e.g., surgery for trauma, pericardial drainage, revascularization for acute myocardial infarction, and antibiotics for sepsis are
needed to treat the underlying cause. In the second phase optimization, the goal is to increase the availability of cellular oxygen, as well as interventions that target hemodynamic
status. Adequate hemodynamic resuscitation reduces inflammation, impaired mitochondrial function, and caspase activation. Measurement of SvO2 and lactate can help guide therapy.
Cardiac monitoring should be considered. In the third phase stabilization, the goal is to prevent permanent organ dysfunction, even after hemodynamic stability has been achieved.
The supply of oxygen to the tissues is no longer a major problem, and the organ of support becomes more relevant. Finally, in the fourth phase de-escalation, the goal is to wean
patients from vasoactive agents and achieve spontaneous polyuria conditions or provoke fluid elimination through the use of diuretics or ultrafiltration to achieve a negative fluid
balance. However, specific treatment of course depends on the type of shock and pathophysiology causes the shock.
Shock HipovolemikHemoragik
In hypovolemic shock indicates the occurrence of bleeding. It is important to know the percentage of blood volume lost as a basis in providing appropriate therapy. In general,
physical examination alone is not enough, but by following the scheme this can be helped. As an assumption that the perceived normal blood volume is 7.5 ml kgbb, the hypovolemic
shock is divided into four groups based on the estimated number of bleeds:
I. 10-15 blood loss from Estimate Blood Volume EBV causes mild
tachycardia and shock has not occurred. II.
Blood loss of 15-25 of EBV 1000-1250ml 70kg arises moderate shock, with tachycardia, systolic pressure and pulse pressure drop, slightly increased
diastolic pressure, slow capillary refill. Urine production is still within normal limits.
III. Blood loss 25-35 EBV 1250-1750 ml 70kg causes severe shock, with
prominent symptoms: the skin is cold, wrinkled, and pale. Blood pressure decreased between 30-40 systolic pressure and pulse pressure and an
increase in diastolic pressure of about 15-20. Vasoconstriction stands out and oliguria develops. Prominent CNS disorder is confusion, which is severe until
stupor occurs. Tachypnea results from secondary metabolic acidosis to hypoxemia, tissue hypo perfusion and anaerobic metabolism. The pulse rate is
greater than or equal to 120x min.
Medical Education Unit Faculty of Medicine Udayana University
41
IV. Blood loss of 35-45 of EBV 1750-2250 ml 70 kg causes very severe
shock, usually a preterminal condition. Unmeasured blood pressure, peripheral pulses are not palpable and carotid pulse is also may not palpable.
Hemorrhagic shock is accompanied by hemodilution and widespread plasma volume expansion at any given time and therefore, the hematocrit does not change for 3 to 4
hours in acute bleeding.
SHOCK CARDIOGENIC Cardiogenic shock CGS is a shock characterized by many factors that interfere with the
normal functioning of the heart, or in particular adverse factors to preload, afterload, contractility, heart rate or heart rhythm. For example right or left ventricular myocardial
infarction, and in situations where cardiac pump failure, or ventricular filling or impaired cardiac discharge.
The above changes occur in hypovolemic hemorrhagic shock and also in cardiogenic shock. In cardiogenic shock caused by myocardial infarction, there is a decrease in mean
arterial pressure, cardiac output, stroke work index, left ventricular diastolic end pressure and volume and venous oxygen content. Heart rate, central venous pressure and
increased arterial and venous oxygen content, and peripheral vascular resistance also increase as a result of compensation. The basic problem is the failure of the heart to
pump blood to peripheral tissue, whatever the cause. Therapy in all types of shock, aimed at the underlying cause while conducting circulatory resuscitation efforts. What is more
important is to save myocardial ischemia and limit the size of infarction through improvement of hemodynamic abnormalities and dysrhythmias. Myocardial
revascularization, balloon angioplasty and thrombolytic therapy are all part of the treatment plan.
SEPTIC SHOCK Incident and Etiology
One of the most common forms of distributive shock is septic shock. The complication of this shock is about 40 of cases by bacteremia gram negative, with a mortality rate of
around 40-90. Septic shock may be caused by bacteria, both gram-negative and gram- positive gram - endotoxin and gram + endotoxin; For example, staphylococci, S.
pneumonia, N.meningitidis, H.gonorrhea or Clostridia, sepsis; Fungi, rickettsia or viruses. Lipopolysaccharides from endotoxin released from gram-negative cell wall
bacteria may be a major part of this syndrome. Septic shock is caused by sequester or misdistribution of normal or high cardiac output in different parts of the body. Tumor
necrosis factor cachectin is known to be a very important mediator of clinical and humoral manifestations in shock caused by endotoxins A- and -O lipid chains or by all
gram-negative bacteria. Vasoactive mediators such as histamine, complement activation, quinine activation especially precancerrein, prostaglandins and possibly other
substances that give rise to vasodilation without compensation to maintain cardiac output. Leucocyte aggregation may cause capillary blockage with inadequate blood flow
results in capillaries. Micro vascular thrombosis is determined by the amount of platelets and clotting factors and manifestations of stimuli of fibrinolysis systems such as DIC and
resulting bleeding. DIC is caused by sepsis associated with a decrease of factor XII, but endotoxin is triggered by intrinsic and extrinsic blood clotting systems.
One theory says that hemorrhagic shock can develop into septic shock as a result of increased permeability of mucous membranes that facilitate enteric bacteria entering the
bloodstream. In this model, severe cellular damage increases the permeability of cell membranes and extracellular fluid displacement into cells associated with impaired cell
Medical Education Unit Faculty of Medicine Udayana University
42
barrier function and disrupts the entry of gram negative or gram-positive bacteria into the bloodstream. This cellular damage can be overcome if resuscitation is successful,
secondary phase bacteremia can be delayed. Survival may be improved if pre shock therapy is anticipated with broad-spectrum antibiotics. Both gram-positive and gram-
negative bacteria appear to cause both cardiovascular abnormalities.
Clinical Manifestations The cardiovascular system is affected by septic shock, at both the myocardial and
peripheral levels. Misdistribution of blood flow followed by myocardial depression, with normal or increased bulk followed by decreased systemic vascular resistance SVR.
Heart rate increased, meanwhile mean arterial pressure, stroke volume, stroke work, oxygen consumption and arterial venous oxygen content all decreased. As already
explained, cardiac output may have been normal or increased. Patients with this condition require large amounts of fluids due to peripheral vasodilation. The decrease of
Left Ventricular Ejection Fraction LVEF and Right Ventricular Ejection Fraction RVEF especially biventricular dilatation occurs 2-4 days after onset of hypotension.
Patients who can be rescued from a septic shock their hemodynamic value will return to their original state of 7-10 days from the onset of septic shock. It has been argued that
what can be saved in septic shock is more likely than cannot be saved with decreased LVEF and left ventricular dilatation, where left ventricular dilatation gives the impression
of a compensatory effort through the Frank-Starling mechanism. The irreversible to normal heartbeat, cardiac output or systemic vascular resistance SVR, whereas
improvement can occur within 24 hours. Mortality can generally be seen from hypotension that is irreversible due to depression of systemic vascular resistance SVR
and cardiac depression so that normal values cannot be maintained within normal limits or above normal until the patient dies. So at first hyper dynamic state with high and
normal cardiac output with low cardiac filling pressure and decreased systemic vascular resistance. The oxygen saturation of the mixed-vein may be normal or low. In high
cardiac output, where abnormal systolic function decreased stroke volume and decreased ejection of left ventricular fraction and ventricular compliance. The
relationship between pulmonary capillary pressure PCWP and left ventricular diastolic end LVEDV volume is not normal. At the next stage, there is a decrease in dynamic
state and the picture resembles a cardiogenic shock. Regarding respiration, where respiratory frequency increases, hyperpnoea, tachypnea and respiratory alkalosis. The
antigen-antibody complex activates the complement system. Septicemia is often followed by ARDS as a complication. Patients with manifest dyspnea, hypoxemia, bilateral diffuse
pulmonary infiltrate, reduction of lung compliance and have usually unchanged pulmonary capillary pressure from the baseline especially if lung function before shock
is normal. Therapy
The primary goal of treating patients with septic shock is eradication removal of causal factors, such as infection, the harmful effects of bacterial toxins or endogenous toxins
from the host and attempts to improve the cardiovascular system and other systems. Many ongoing research experiments to study drugs to counteract the effects of toxins on
septic shock. For the practical use of anesthesia, most of these are clinically unimportant and are mentioned only for the completeness of the data. Currently, monoclonal
antibodies as part of gram-negative bacteria, naloxone, prostaglandin inhibitors, lipid X, tumor necrosis factor antibodies TNF, genetically engineered protease inhibitors and
other recombinants or synthetic protease inhibitors. Cardiovascular support for septic shock patients consists of fluids and vasopressors required.
Medical Education Unit Faculty of Medicine Udayana University
43
Fluid is required for optimization of preload and cardiac output above normal values so that MAP returns to the baseline if possible or at least initially 60 mmHg. Pulmonary
capillary pressure PCWP is optimally 12-15 mmHg and should be monitored by invasive techniques with pulmonary artery catheter. The selected fluid type did not seem
to provide much benefit with respect to the expected results, although experimental experiments in experimental animals with septic shock resulted in a significant
improvement in cardiac output, Lung Water Extravascular Extension PVR and Venous Admixture VR vascular cavity when given Dextran 70 compared to Ringers Lactate.
Fluid resuscitation has shown effective results for increasing oxygen delivery DO2 and oxygen consumption VO2 in septic shock.
The arrangement of ventricular function following Frank-Starling law and the category of patients corresponding to the functional can assist in decision-making of inotropic
drugs, diuretics and vasopressors for patient resuscitation. Optimal oxygen transport through correction of anemia and also followed by improvement in serum albumin levels
of at least 2 g 100 ml is important as adjunctive therapy. If only with volume correction alone the hypotension is not corrected, while maintaining the pulmonary capillary
pressure PCWP greater than or equal to 15mmHG, the vasopressor may be added cautiously, starting with low dopamine doses 1-3μg kg min and norepinephrine If
large doses of dopamine are ineffective to increase mean arterial pressure MAP or side effects tachycardia, dysrhythmias. If norepinephrine is also ineffective, it should be
substituted with epinephrine or dobutamine or when low cardiac output is required to use beta-mimetic adrenergic agonism.
OBSTRUCTIVE SHOCK
Obstructive shock is a form of shock associated with physical obstruction of the great vessels or the heart itself. Pulmonary embolism and cardiac tamponade are
considered forms of obstructive shock. Obstructive shock has much in common with cardiogenic shock, and the two are frequently grouped together. It was described as
involving obstruction to flow in the cardiovascular circuit and characterized by impairment of diastolic filling or excessive afterload. The consequent obstruction of blood
flow into or out of the heart causes a decrease in cardiac output, and hence inadequate oxygen delivery, which is manifest by the classic signs and symptoms of the shock state.
Obstructive shock is rare in pediatrics, though the most common causes generally include tension pneumothorax, cardiac tamponade, and pulmonary embolism. Also included in
this category physiologically, and more specific to pediatrics, are congenital heart lesions characterized by left ventricular outflow tract obstruction, including critical aortic
stenosis, coarctation of the aorta, interrupted aortic arch, and hypoplastic left heart syndrome. Herein, we will briefly review the major causes of obstructive shock found in
children.
Tension Pneumothorax A pneumothorax is defined as the accumulation of air in the pleural space, a cavity
that is normally filled with a small amount of pleural fluid. It can be spontaneous more common in adolescent males or secondary to underlying lung pathology, such as trauma
both penetrating and blunt trauma, asthma, cystic fibrosis, and pneumonia. Also included in this subcategory are iatrogenic causes such as barotrauma during positive
pressure ventilation or during placement of central venous catheters in the chest vessels.
The incidence of secondary pneumothorax in pediatric patients is not well described, however, in critically ill children requiring mechanical ventilation it is reported to be 4-
15. Notably, the incidence of secondary pneumothorax in mechanically ventilated pediatric patients has declined markedly since the introduction of protective lung
Medical Education Unit Faculty of Medicine Udayana University
44
strategies. Pneumothoraces can be well tolerated in some patients, though signs and symptoms of obstructive shock can develop if the pneumothorax is under tension. In this
scenario, the
air in the pleural space continues to collect under a one-way or ball valve effect, such that air
enters during inhalation, but cannot exit during exhalation. Eventually, enough air accumulates such that the intrathoracic pressure of the affected hemi-thorax equilibrates
with atmospheric pressure, leading to complete lung collapse or atelectasis. Air under tension also causes a shifting of the mediastinum, compression and total collapse of the
lung and great vessels, thereby compromising both cardiovascular and respiratory function. Studies in animal models have shown that the early clinical features of a tension
pneumothorax include hypoxemia, tachycardia, and respiratory distress due to compression and collapse of lung segments. As mechanical compromise of venous
structures develops, there is a drastic and profound reduction in venous return to the heart as well, clinically manifested by symptoms of shock and poor perfusion. Thus, overt
hypotension may be a late sign. Complete occlusive mechanical compression is suggested by equalization of the Mean Intrathoracic Pressure MIP and Central Venous Pressure
CVP, which is a very late event and results in cardiovascular collapse. Treatment of a tension pneumothorax requires emergent needle decompression, usually performed by
placing a sterile needle in the second intercostal space along the midclavicular line. Definitive treatment requires thoracostomy tube placement.
Cardiac Tamponade The pericardial sac around the heart is relatively noncompliant, and the accumulation
of even small amounts of fluid can be sufficient to produce cardiac tamponade physiology. While acute pericardial fluid changes are usually symptomatic, the chronic
accumulation of fluid may occur with little to no hemodynamic derangements, as the pericardium slowly stretches to accommodate the excess volume over time. Pericardial
effusions can develop as a result of any type of pericardial inflammation i.e., pericarditis, causing a range of physiologic perturbations along the spectrum of minor
flu-like symptoms i.e., manifestations of the pericarditis itself to a life-threatening state characterized by cardiac tamponade and obstructive shock. Historically, the most common
cause
of pericardial effusions was infectious pericarditis, though a recent review suggests that
idiopathic and neoplastic causes are much more frequent due to the success of childhood vaccinations. Other common causes include postpericardiotomy syndrome following
cardiac surgery for congenital heart disease and trauma, most often causing hemopericardium. Effusions may also develop as a result of a central line that erodes
through the thin wall of the right atrium, a phenomenon that appears primarily limited to neonates and young infants. The pathophysiology of cardiac tamponade is welldescribed.
Briefly, increased intrapericardial pressure limits venous return to the heart and causes right ventricular compression. There is a progressive decline in right ventricular end-
diastolic volume as diastolic filling lessens, worsening cardiac output. In severe tamponade,
venous return during inspiration into the compressed right ventricle bows the interventricular
septum into the left ventricle, further diminishing systemic cardiac output. As pericardial pressure increases and surpasses ventricular end-diastolic pressure, the ventricular
volumes grow smaller and smaller and cardiac output worsens. Tamponade is a clinical diagnosis and classically, patients with critical cardiac tamponade present with Beck’s
triad of symptoms including hypotension, quiet “muffled” heart sounds, and raised
Medical Education Unit Faculty of Medicine Udayana University
45
jugular venous pressure. Patients may present with dyspnea, compensatory tachycardia, and poor perfusion. On auscultation, a friction rub and distant heart sounds may be
present. Pulsus
paradoxus, defined as a decline in systolic blood pressure greater than or equal to 10 mm Hg during inspiration, results from the inspiratory reduction in pleural pressure that
produces a fall in left ventricular output and arterial systolic pressure. An electrocardiogram may show electrical alternans due to the heart swinging within the
large effusion. Formal evaluation with an urgent echocardiogram should be performed in those patients with symptoms suspicious for cardiac tamponade. However, emergent
management should not wait for echocardiography and is frequently based upon the recognition of tamponade physiology in the appropriate clinical context.
Pericardiocentesis is the lifesaving procedure of choice for children with cardiac tamponade and can safely be done with bedside echocardiographic guidance. Medical
stabilization with fluid resuscitation and inotropic support is temporary at best and somewhat
controversial as
fluid resuscitation may worsen tamponade physiology, especially in children who are either
normovolemic or hypervolemic. In the latter scenario, fluid administration will increase intracardiac pressures further, hence increasing intrapericardial pressures and worsening
tamponade.
Pulmonary Embolism Pulmonary embolism PE is uncommonly diagnosed in children, making its true
incidence difficult to determine. However, the incidence of PE does appear to be on the rise, though this may be due to a heightened index of clinical suspicion and better
recognition by pediatric providers. Alternatively, it may be due to the fact that more children
are surviving from previously fatal conditions that place them at an increased risk for
developing PE, such as congenital heart disease and malignancy. In addition, more children are requiring central venous catheterization for vascular access, a major risk
factor for venous thromboembolism VTE, which can lead to a PE. PE is frequently fatal and difficult to diagnose. In a recent literature review comparing pediatric PE with adult
PE, pediatric cases were more often diagnosed at autopsy and were associated with a higher mortality rate than adults. The clinical presentation often is confusing, perhaps
compounded by the fact that very few pediatricians have much experience with this disorder.
Results of
screening tests, such as oxygen saturation, electrocardiography, and chest radiography, may be
normal. Thus, a high index of clinical suspicion is necessary. Evaluation should be performed with spiral computed tomography CT venography, which is now widely
considered the study of choice due to its 90 sensitivity and specificity in adults. Ventilation Perfusion VQ scans are also available but are more difficult to obtain and
to interpret in pediatrics. As a cause of cardiogenic shock, a massive PE has a profound impact upon gas exchange and hemodynamics. Obstruction to flow through the
pulmonary artery results in increased dead space ventilation where affected lung segments are ventilated but not perfused, observed clinically as a substantial decrease in
the end-tidal CO2 ETCO2 that no longer reflects arterial PCO2. A widened alveolar- arterialgradient A-a is present as well. The mechanism for hypoxemia likely involves
several mechanisms. In some pediatric patients, an intracardiac right-to-left shunt through a patent foramen ovale may be present and as right atrial pressure increases and
eventually exceeds the left atrial pressure, deoxygenated blood can shunt directly into the systemic circulation. In addition, VQ mismatching is compounded by the accompanying
Medical Education Unit Faculty of Medicine Udayana University
46
fall in cardiac output that results from massive PE, leading to mixed venous desaturation. PE increases the right ventricular RV afterload, resulting in an increase in
the RV end-diastolic volume EDV. The increase in RVEDV adversely affects left ventricular hemodynamics through ventricular interdependence. Specifically, the
interventricular septum bows into the left ventricle LV and impairs diastolic filling, resulting in decreased LV preload and subsequently diminished cardiac output and
hypotension. These physiologic phenomenon are manifested by respiratory distress, hypoxia, and decreased cardiac output with signs of shock.
Treatment of an acute pulmonary embolus in children should begin with initiation of a heparin infusion with or without fibrinolytic agents such as tPA, depending on the
child and the extent of the clot. In the resolution period, the child will then warrant at least 3-6 months of anticoagulation with low molecular weight heparin LMWH or warfarin.
MONITORING SHOCK Hemodynamic Monitoring
Patients with shock are a critical condition and require invasive hemodynamic monitoring especially in cases where vasoactive drugs are used for resuscitation or are
used to support the cardiovascular system. Generally, it is classified into routine and exceptional or non-routine monitoring. Regular monitoring are used in patients with
critical condition who receive get state of the art care in the intensive care room. Extraordinary or non-routine monitoring are used in patients who need to be monitored
continuously in the ICU, for example in the extravascular lung water.
Meanwhile, blood pressure changes must be correctly measured in shock because blood flow is determined by the relationship between cardiac output and systemic
vascular resistance, but in shock, blood pressure should be measured by continuous monitoring with beat to beat arterial pressure. To be able to see the rapid changes can be
installed sphygmomanometer or Doppler placed on the artery line. In addition, monitoring of all patients includes: heart rate and rhythm, breath frequency, body
temperature, right and left heart pressure, ECG and hematocrit. In the installation of arterial catheters that settle arterial blood samples can be taken in a peiodic manner to
determine the state of electrolytes and the properties of blood clotting and arterial lactate levels. The catheter insertion into the pulmonary artery may be excellent for assessing
pulmonary artery pressure, pulmonary artery occlusion pressure, cardiac output and other parameters including vascular resistance. Pulmonary artery catheters have the ability to
assess venous blood saturation, particularly in patients with cardiogenic shock. Central venous pressure monitoring is sometimes used to determine or determine the amount of
blood lost, given that a 500-800ml blood loss for 70kg weight will lower central venous pressure by about 7cmH2O.
Patients with shock who also get general anesthesia, decreased arterial blood pressure may be faster than patients who are not publicly anesthetized because the compensation
of tone sympathetic nervous system is removed by anesthesia and in this patient, invasive blood pressure monitoring by continuously beat to beat, will be very helpful. Korotkoff
sounds decreased or inaudible in severe shock which received general anesthesia and subsequently assisted with an invasive monitor.
Assessment of electrolytes and hematocrit from arterial blood samples can provide important information during resuscitation and shock management. Assessment of blood
volume and circulatory function can be better assessed in patients who have serial laboratory results. Blood loss of about 3-4 times in acute bleeding can lead to significant
changes in hematocrit. The decrease in capillary hydrostatic pressure with bleeding is characterized by increased intravenous interstitial fluid absorption. As a result,
Medical Education Unit Faculty of Medicine Udayana University
47
intravascular fluids multiply and hematocrit decreases as a result of fewer percentage of red blood cells in intravascular fluid. It should still be assessed during shock therapy and
monitoring of fixed hemodynamic variables, and there is no evidence to suggest that simple correction by assessment of common parameters can result in greater outcomes or
lower morbidity.
Of the hemodynamic variables, two things that need attention in the assessment of shock sufferers are: oxygen delivery and oxygen consumption.
Oxygen delivery DO2 is the result of arterial oxygen content and cardiac index. DO2 = CaO2 x CI x 10, where CaO2 = 1.39 x Hgb x saturation + PaO2 x 0.003 and
CI = cardiac output body surface area. The normal value for DO2 is 520-720ml min m2.
Oxygen consumption VO2 is the result of arterial oxygen content minus venous oxygen content and cardiac index times 10 VO2 = CaO2 - CVO2 x CI x 10. The
normal value for VO2 is 100-180ml min m2. VO2 describes the sum of all oxidative metabolic outcomes and thus is a measure of total body metabolism.
Of the hemodynamic variables that need attention include the counting of shunt fraction Q2 Qt and A-aDO2 or the oxygen difference between alveolar and arterial. The
direct flow of the pulmonary artery catheter is a therapeutic change in shock sufferers with modification of Starlings law. In general, it is used given that the mean pulmonary
artery pressure of about 5-10mmHg is greater than the pulmonary capillary wedge pressure PCWP, and the pulmonary arterial diastolic pressure is approximately 0-
3mmHg greater than PCWP. PCWP is almost identical with left atrial pressure or diastolic final pressure except in cases with mitral stenosis, where the left ventricular end
diastolic pressure LVEDP can not be determined or estimated from pulmonary capillary wedge pressure PCWP. Cardiac output may also be demonstrated by using
thermodilatory techniques if there is no intracardiac shunt left to right or right to left. Central Vein Pressure
Interpreting Central Venous Pressure CVP separately on the shock has a small value of significance. Central venous pressure response to fluids is questionable, although
important as a guide in therapy. If the central venous pressure changes little or does not change with the increase in pulse pressure after fluid administration, subsequent fluid
administration may be indicated. If CVP increases after fluid bolus or doubt, subsequent fluid administration may be discontinued and to achieve the desired blood pressure, need
to be pharmacologically or otherwise. Pulmonary Arterial Diastolic Pressure PAdP
PAdP is usually worth about 1-2mmHg greater than pulmonary capillary pressure PCWP in the absence of pulmonary hypertension. If PAdP is reduced PCWP greater
than 5mmHg, it means pulmonary hypertension. PAdP changes are used to assess the benefits of the effects of fluid therapy on shock.
Lactate levels
Monitoring arterial lactate levels is important in shock and associated with prognosis. In shock, lactate levels increase and the lactate-pyruvate ratio also increases. Arterial
blood lactate levels are greater than 2.5mM L, statistically the likelihood of survival decreases dramatically and at 4.5mM L, the chance of survival is only about 50.
When more than 7.0mM L the chance to survive less than 10.
Patients who can be rescued from shock seem to have low lactate levels compared with those that do not and also appear to decrease lactic acid at least 10 per hour
immediately after therapy, while patients who can not be saved by therapy, lactate levels do not decrease. The level of lactate is expressed in milligrams of milliliters or milliliters
of perliter. Apparently, lactate levels may be measured from arterial blood or from a
Medical Education Unit Faculty of Medicine Udayana University
48
central vein of the pulmonary artery with the same degree of accuracy. One study showed that there was no correlation between arterial blood lactate levels and oxygen delivery
changes in septic shock or non septic shock. However, continuous monitoring of lactate levels is very useful to know the severity of shock.
SHOCK IN PEDIATRIC I Nyoman Budi Hartawan
Abstracts Shock is divided into three major categories: hypovolemic, cardiogenics, and distributive,
with a degree of overlap. Hypovolemic shock is result of inadequate circulating blood volume owing to blood or fluid loss or of insufficent fluid intake. Cardiogenic shock occurs
when cardiac compensatory mechanisms fail and may occur in infants and young children and in patients with preexisting myocordinal disease or injury. Distributive shock, such as
septic and anaphylactic shock, is associated with peripheral vasodilations, arterial and capillary shunting past tissue beds with pooling of venous blood, and decreased venous
return to the heart. Shock is clinical diagnosis, but its recognition remain problematic in children. Shock may be present long before hypotention occurs. Children will often maintain
their blood pressure until late stage of shock; therefore, the presence of systemic hypotention is not required to make the diagnosis of shock in chldren, as it is an adult. For example septic
shock in pediatric patients has been define as tachycardia which may be absent in the hypothermic patient with signs of decreased perfusion, including decreased peripheral
pulses, compared with central pulses, altered alertnes, flash capillary refill or capillary refill 2secs, mottled or cool extremities, and decrease urine output. Hypotention ia a sign of late
and decompensated shock in children. If present in a child with these other featur
Lecture 8 : CARDIAC ARREST AND CARDIOPULMONAR RESCUSTATION IGN Mahaalit Aribawa
Objective :
1. To describe etio-pathogenesis and pathophysiology of cardiac arrest
2. To implement a general strategy in the approach to patients with cardiac arrest
through history, physical examination and special tehnique investigations. 3.
To manage by assesing, provide initial resuscitation and refer patient with post resuscitation cardiac arrest
4. To describe prognosis patient with post cardiac arrest
Abstract Medical emergencies that threaten lives can occur anywhere, anytime and to anybody. It
can be because of a disease or due to road accident, drowning, poisoning and others that are capable of causing respiratory and cardiac arrest.
Air way obstruction such as hypoventilation, respiratory arrest, shock, even cardiac arrest, causes death quickly if fast and appropriate help is not given. Death of patients due to
the causes mentioned above can be avoided if resuscitation is done immediately on the spot. Permanent brain damage can occur if blood circulation has stopped for more than a few
minutes now it has been agreed more than 4-6 minutes or after a trauma with severe
Medical Education Unit Faculty of Medicine Udayana University
49
hypoxia or loss of lots of blood which are not corrected. If resuscitation is given immediately and correctly brain death can be avoided and the patient recovers completely.
General strategy to obtain the diagnosis of acute respiratory failure and cardiac arrest, is done by a subjective approach or anamnesis and objective approach with physical
examinations and few other diagnostic criteria to find the primary signs and symptoms of respiratory and cardiac arrest. The diagnosis of respiratory and cardiac arrest should be done
immediately and accurately. Delay in diagnosis will cause delay in resuscitation and this will cause death to even the patients with higher living chances.
Resuscitation can be done anywhere, anytime, with or without equipment by trained whether public or health personnel. CPR cardiopulmonary resuscitation is an effort of
medical emergency to cure respiratory function and circulation which has failed drastically on a patient that has the chances of living.
For an immediate failure, the lung and heart are in good shape, compared to those due to chronic diseases, that cure is possible. Besides that, how are we to know a patient’s condition
that still has a chance of living? To know the prognosis, a senior doctorconsultant with knowledge, experience and mature considerations is needed.
Lecture 9 :EMERGENCY TOXICOLOGY AND POISONING Agus Somya
LEARNING OBJECTIVE 5.
To describe general approach of acute intoxicationpoisoning 6.
To describe general management of acute intoxicationpoisoning 7.
To describe management of methanol intoxication 8.
To describe management of opiate intoxication 9.
To descripe management of organophospate intoxication 10.
To describe management of caustic intoxication
ABSTRACT General approach and management of acute intoxicationpoisoning
Acutely poisoned patients are commonly encountered in Emergency Centres. Acute intoxicationpoisoning accidental or intentional requires accurate assessment and prompt
therapy. Early identification of the involved toxins is crucial and the majority will be identified by a thorough history and physical examination. An ABC-approach should be
followed ensuring a protected airway, adequate ventilation and hemodynamic stability. Supportive and symptomatic care remains the cornerstone of treatment. A stepwise approach
may be followed to decrease the bioavailability of toxins. Indications, contra-indications, risks and dosage regimens are describe for decontamination procedures including both
termination of topical exposures and decreasing exposure to ingested toxins. Furthermore, procedures to increase the elimination of toxins and a short section covering specific toxins
and their antidotes are also included
Organophosphat poisoning
Organophosphorus pesticide self-poisoning is a major clinical and public-health problem across much of rural Asia. Of the estimated 500 000 deaths from self-harm in the
region each year, about 60 are due to pesticide poisoning.
Medical Education Unit Faculty of Medicine Udayana University
50
Organophosphorus pesticides inhibit esterase enzymes, especially acetylcholinesterase in synapses and on red-cell membranes, and butyrylcholinesterase in
plasma. Although acute butyrylcholinesterase inhibition does not seem to cause clinical features, acetylcholinesterase inhibition results in accumulation of acetylcholine and
overstimulation of acetylcholine receptors in synapses of the autonomic nervous system, CNS, and neuromuscular junctions. The subsequent autonomic, CNS, and neuromuscular
features of organophosphorus poisoning are well known
Clinical features of organophosphorus pesticide poisoning including:
- overstimulation of muscarinic acetylcholine receptors in the parasympathetic system
Bronchospasm, Bronchorrhoea, Miosis, Lachrymation, Urination, Diarrhoea, Hypotension, Bradycardia, Vomiting, Salivation.
- overstimulation of nicotinic acetylcholine receptors in the sympathetic system:
Tachycardia, Mydriasis, Hypertension, Sweating. -
overstimulation of nicotinic and muscarinic acetylcholine receptors in the CNS: Confusion, Agitation, Coma, Respiratory failure.
- overstimulation of nicotinic acetylcholine receptors at the neuromuscular junction:
Muscle weakness, Paralysis and Fasciculations Treatment includes resuscitation of patients and giving oxygen, a muscarinic
antagonist usually atropine, fluids, and an acetylcholinesterase reactivator an oxime that reactivates acetylcholinesterase by removal of the phosphate group. Respiratory support is
given as necessary. Gastric decontamination should be considered only after the patient has been fully resuscitated and stabilised. Patients must be carefully observed after stabilisation
for changes in atropine needs, worsening respiratory function because of intermediate syndrome, and recurrent cholinergic features occuring with fat-soluble organophosphorus.
Caustic agent intoxication
Caustic ingestions may cause widespread injury to the lips, oral cavity, pharynx, and the upper airway. The effect that these agents have on the esophagus accounts for most of the
serious injuries and long-term complications. The nature of the injury caused by caustic ingestion is determined by a number of factors including the identity of the agent, the amount
consumed, the concentration, and the length of time the agent is in contact with a given tissue. Caustic materials cause tissue injury by chemical reaction. These materials are
generally acidic or alkali. Usually, acids with pH less than 3 or bases with pH greater than 11 are of the greatest concern for caustic injury.
The esophagus is the site of most long-term sequelae from caustic ingestion. Injury to the esophagus is rapid, as described above, for both acids and alkalis, but this acute tissue
disintegration and deep tissue penetration may continue for hours. Injury progresses within the first week after ingestion, with inflammation and vascular thrombosis. A developing ulcer
with fibrin crust will be seen in a few days. Granulation tissue develops between 2 to 4 days and is revealed under shed necrotic tissue by days 15 to 20.
After caustic ingestion, patients may present with a combination of many symptoms or none at all depending on the nature of the agent, the specifics of the ingestion quantity,
intent, timing, and what tissues were affected. Induction of emesis should be avoided to prevent further injury as the agent is
vomited. Neutralization of the caustic material should be avoided because of the potential for causing an exothermic injury, which may worsen an existing injury.
Opioid intoxication
Medical Education Unit Faculty of Medicine Udayana University
51
Opioid analgesic overdose is a preventable and potentially lethal condition that results from prescribing practices, inadequate understanding on the patients part of the risks
of medication misuse, errors in drug administration, and pharmaceutical abuse. Three features are key to an understanding of opioid analgesic toxicity. First, opioid analgesic
overdose can have life-threatening toxic effects in multiple organ systems. Second, normal pharmacokinetic properties are often disrupted during an overdose and can prolong
intoxication dramatically.
3
Third, the duration of action varies among opioid formulations, and failure to recognize such variations can lead to inappropriate treatment decisions,
sometimes with lethal results Opioids increase activity at one or more G-protein–coupled transmembrane
molecules, known as the mu, delta, and kappa opioid receptors. The presence of hypopnea or apnea, miosis, and stupor should lead the clinician to
consider the diagnosis of opioid analgesic overdose, which may be inferred from the patients vital signs, history, and physical examination. In patients with severe respiratory depression,
restoration of ventilation and oxygenation takes precedence over obtaining the history of the present illness or performing a physical examination or diagnostic testing
Naloxone, the antidote for opioid overdose, is a competitive mu opioid–receptor antagonist that reverses all signs of opioid intoxication.
Metanol Intoxication
Methanol methyl alcohol, CH3OH is the simplest type of alcohol, very light, volatile, colorless, flammable, distinctive smell a little sweeter than etanol.3 methanol is used
for industrial products, and also as a mixture with ethanol to drink Traditional hard. Industrial products that use methanol is a liquid car cleaner, solvent paints, cleansers,
perfumes, car fuel and other industrial products.
Methanol poisoning is a major disruption to the central nervous system, the optic nerve and basal ganglia. The formic acid acts cause toxicity to the eye by inhibiting
cytochrome oxidase in the optic nerve, interrupting the flow axoplasma. While substances that contribute to the occurrence of metabolic acidosis and decreased plasma bicarbonate is
formaldehyde, formic acid and lactic acid.
Toxic doses of methanol ranges between 15-500 cc of methanol solution containing 40 to 60-600 cc of methanol. Methanol poisoning begins with mild drunk and sleepy.
Followed by a latent phase 40 minutes - 72 hours which is the period without symptoms, due to the slow production of formaldehyde and formic acid. This phase was followed by the
appearance of metabolic acidosis, anion gap and impaired of vision. Visual disturbances such as blurred to decrease visual acuity. In the later phase of seizures, coma and death. Slower
onset of methanol poisoning if the patient is also taking ethanol simultaneously.
On laboratory examination found an increase in serum osmolality, anion gap, serum lactic acid and metabolic acidosis. Definitive diagnosis and monitoring of treatment response
based on the examination of serum methanol levels. Specific Management of acute methanol poisoning include:
- Inhibitors of alcohol dehydrogenase
- Treatment with Co-factor: folinic acid 50 mg IV or folic acid 50 mg IV every 6
hours. -
Sodium Bicarbonate -
Hemodialis: Hemodialis is the fastest way of issuing metabolic toxic acid and methan
Medical Education Unit Faculty of Medicine Udayana University
52
Lecture 10 : PREGNANCY INDUCED HYPERTENSION
Gede Megaputra OBGYN Team
Objective : 1. Define pregnancy induced hypertension
2. Review appropriate fetalmaternal assessment 3. Discuss appropriate anti – hypertension and anti – seizure therapy
4. Recognize when and how to transport patient with pregnancy induced hypertension
Hypertensive disorders in pregnancies are the leading causes of maternal death in emerging countries. All caregivers must be able to promptly recognized the signs, symptoms and
laboratory findings of gestational hypertension with or without proteinuria and with other adverse manifestation. Caregivers must appreciate fully the seriousness of gestational
hypertension, its potential for multi – organ involment and the risk for perinatal and maternal morbidity and mortality. The appropriate management of gestational hypertension may vary
based on the availability of resources. In this lecture student will discuss such as : the classification and definition of hypertensive disorders in pregnancy; management and
treatment of gestational hypertension.
Severe gestational hypertension is an obstetrical emergency, which requires prompt recognition, stabilization of mother and fetus and multi – disciplinary approach to
management and treatment
Lecture 11 : SHOULDER DYSTOCIA
Endang Sriwidiyanti OBGYN Team
Objective 1. Define shoulder dystocia
2. Review appropriate fetalmaternal assessment 3. Discuss the risk factors of shoulder dystocia
4. Discuss the complications of shoulder dystocia 5. Discuss appropriate management of shoulder dystocia
Shoulder dystocia is one of emergency problems during delivery. Following the delivery of the head, there is impaction of the anterior shoulder on the symphysis pubis in the
AP diameter, in such a way that the remainder of the body cannot be delivered in the usual manner. More than 50 of cases shoulder dystocia occur in the absence of any identified risk
Medical Education Unit Faculty of Medicine Udayana University
53
factor. The student will discuss the assessment of shoulder dystocia, the complication for fetus and mother, identification of risk factor, and management
10.1. DEFINITION
After the birth of the head, external rotation will take place which causes axis of the head to be on the normal axis to the spine. Generally shoulder will be on the oblique axis
under the pubic ramus. Pushing of the mother will cause the anterior shoulder become under the pubis. If the shoulder fails to hold a rotation of adjusting to the axis of tilted pelvis and
remain in the anteroposterior position, the baby will most collision front shoulder to the symphysis.
1,2
Shoulder dystocia is mainly caused by deformities of the pelvis, the failure of the shoulder to folded into the pelvis eg on macrosomia caused by active phase and short
second stage of labor in multiparas so the descence of the head is too quickly, causing the shoulder does not fold through the birth canal or head has through the middle pelvis after a
prolong of the second stage of labor before the shoulder successfully folded into the pelvis.
3
The main mechanism behind the occurrence of shoulder dystocia is the reten- tion of
the anterior shoulder behind the pubic symphysis, while the posterior shoulder is usually located in the maternal pelvis Figure 10.1.. In rare situations, both shoulders are retained
above the pelvic brim.
4
Figure 10.1. The main mechanism behind the occurrence of shoulder dystocia –
retention of the anterior fetal shoulder above the pubic symphysis
10.2. INCIDENCE
An over- all incidence between 5.8-7 in 1000
of vaginal deliveries is reported in the largest observational studies
4
, while others studies find incidence of 1-2 in 1000 birth and 16 in 1000 birth of baby weight more than 4000 gram.
3
Medical Education Unit Faculty of Medicine Udayana University
54
10.3. RISK FACTORS
4
The main risk factors for shoulder dystocia are listed in Table 10.1. Previous shoulder dystocia stands out as a major risk factor for recurrence, and it is reported to be 10
times higher than in the general population, for an overall incidence of 1–25. The anatomical characteristics of the maternal pelvis that predispose to shoulder dystocia and
may cause it to be recurrent in nature are poorly understood. When additional risk factors are present, such as maternal diabetes or suspected fetal macrosomia or when previous fetal
injury occurred in association with shoulder dystocia, serious consider- ation should be given to elective caesarean delivery, and this option should be discussed with the mother.
4
Another major risk factor is fetal macrosomia, and when coexistent with poorly controlled maternal diabetes, an additional 2–4-fold risk is present, posed by the increased
diameter of the fetal shoulders.
4
Table 10.1. Main Risk Factors for Shoulder Dystocia
4
Risk Factor Previous shoulder dystocia
Fetal macrosomia and its associated risk factors Pre-existing or gestational diabetes
Maternal obesity Excessive weight gain during pregnancy
Post-term pregnancy Slow progress of labour vaginal delivery
Prolonged first andor second stage Need for labour acceleration
Instrumental
The majority of cases of shoulder dystocia occur in pregnancies that have no risk factors, and when one is present, the majority of cases do not develop this complication.
There is therefore wide agreement within the medical community that shoulder dystocia is generally an unpredictable situation. Nevertheless, identification of risk factors is useful for
anticipating of the situation, so that an experienced team can be on hand at the time of delivery.
4
10.4. COMPLICATIONS
Complications of shoulder dystocia are described in Table 10.2. The most frequent
complication of shoulder dystocia is brachial plexus injury, of which Erb’s palsy is the usual presentation. The latter manifests by a characteristic position of the affected arm that
hangs by the side of the body and is rotated medially. The forearm is usually extended and pronate Fig. 10.2. It affects about 0.15 of all births, and in some countries, the incidence
appears to be decreasing. Older studies report brachial plexus injury to occur in 2–16 of shoulder dystocias, but recent data from centres performing regular staff training refer that
this can be reduced to about 1.3 . Brachial plexus injury appears to be related mainly to the traction force applied on the fetal head. Improved awareness of the fact and simulation-based
training of the force that can be safely applied to the fetal head may be responsible for the decreasing incidence of this complication.
4
Medical Education Unit Faculty of Medicine Udayana University
55
Of all brachial plexus injuries diagnosed at birth, the majority disappear after treatment, and only 10–23 remain after 12 months. In the majority of cases of residual
paralysis, some degree of recovery is achievable after surgery.
4
Shoulder dystocia is also a cause of perinatal mortality, although the incidence
appears to have decreased in the last decades. Confidential enquiries carried out in the United Kingdom indicate that it may be responsible for about 8 of intrapartum fetal deaths.
The main cause of perinatal death is acute fetal hypoxiaacidosis.
4
There is uncertainty about how many minutes may elapse before the fetus is at risk of injury from acute hypoxiaacidosis. The phenomenon is probably faster when there are
nuchal cords and when cord clamping takes place before the shoulders are released.
4
Figure. 10.2 Newborn with a right arm
position typical of Erb’s paralysis.
4
Compression of fetal neck vessels may also play an important part in the patho- physiological mechanism, and it may be the main cause of cerebral injury when no nuchal
cords are present. Again, umbilical blood gas values may not translate the severity of hypoxiaacidosis occurring in the brain, and hypoxic-ischaemic encephalopathy has been
documented in cases with only moderate acidemia on cord gas analysis. In a small but well- documented observational study, no cases of hypoxic- ischaemic encephalopathy were found
when resolution took less than 5 min, and only mild cases of hypoxic-ischaemic encephalopathy were reported when it lasted 5–9 min. Serious complications of
hypoxiaacidosis were only described in one case where more than 12 min elapsed.
4
Table 10.2. Complications of Shoulder Dystocia
4
Newborn Complications Death 8
Asphysxia and its complications
Medical Education Unit Faculty of Medicine Udayana University
56
Fracture of Clavicula, humerus Brachial Plexus Injury most common
Maternal Complications Postpartum haemorrhage 11
Uterine Rupture Bladder rupture
Dehiscence of pubic symphisis Sacro-iliac joint dislocation
Although there are no certainties as
to the time that may elapse before the fetus is at risk of injury from hypoxiaacidosis, it seems wise not to clamp nuchal cords after the head is delivered unless there is no other
alternative and to attempt resolution preferably within 5 min. When 12 min have elapsed, fetal prognosis is likely to be poor. Different timings must be considered when fetal
oxygenation is already compromised before the occurrence of shoulder dystocia or when there is fetal growth restriction.
4
Rarer complications of shoulder dystocia are fractures of clavicle and humerus, the
majority of which are iatrogenic in nature, consequent to the manoeuvres used for resolution of the situation, and they usually heal without sequelae after immobilisation.
4
The most frequent maternal complications are vaginal and perineal lacerations, and
some studies report anal sphincter lacerations to occur in about 4 of shoulder dystocia cases.
4
Postpartum haemorrhage affects about 11 of cases and can be caused by birth
canal lacerations and more frequently by uterine atony. Rare cases of uterine rupture, bladder rupture, dehiscence of the pubic symphysis and sacroiliac joint dislocation have also been
described.
4
10.5. DIAGNOSIS
3
• Turtle’ sign
• Prolonged second stage of labour
• Fail to deliver the baby with maximal effort and proper management
Medical Education Unit Faculty of Medicine Udayana University
57
Figure. 10.3 Turtle sign, with the lower structures of the fetal head depressing the maternal perineum
4
10.6 MANAGEMENT
Requirement
3
Maternal vital condition is sufficient to work together to completing deliveries The mother has the ability to pushing
The passage and the pelvic outlet are adequate for the babys body accommodation The baby is still alive or are expected to survive
Not monstrum or congenital abnormality that prevents the delivery of baby
The management mnemonic ALARMER 1. Principles : Do not 4 “P” :
Panic
Pulling the head of the baby
Pushing the fundal of uterine
Pivoting the head of the baby with coccygeus as fulcrums
2. Ask For Help :
The mother of patient
Husband
Midwife
Physician in charge or other paramedic
3. Lift the buttock- McRobert’s Maneuver
The McRoberts maneuver was described by Gonik and associates 1983 and named for William A. McRoberts, Jr., who popularized its use at the University of Texas at
Houston. The maneuver consists of removing the legs from the stirrups and sharply flexing them up onto the abdomen Fig. 10.4. Gherman and associates 2000 analyzed
the McRoberts maneuver using x-ray pelvimetry. They found that the procedure caused straightening of the sacrum relative to the lumbar vertebrae, rotation of the symphysis
pubis toward the maternal head, and a decrease in the angle of pelvic inclination. Although this does not increase pelvic dimensions, pelvic rotation cephalad tends to free
the impacted anterior shoulder. Gonik and coworkers 1989 tested the McRoberts position objectively with laboratory models and found that the maneuver reduced the
forces needed to free the fetal shoulder.
4
Medical Education Unit Faculty of Medicine Udayana University
58
Figure 10.4. a. McRoberts Maneuver, the maneuver consists of removing the legs from the stirrups and sharply flexing the thighs up onto the abdomen. b. “The McRoberts
maneuver and the assistant is also providing suprapubic pressure simultaneously arrow.
2,4
4. Anterior Disimpaction
4.1. Suprapubic Pressure Manuver Massanti
• Suprapubic pressure on the babys anterior shoulder toward the chest of the
baby.
Figure 10.5. Suprapubic Pressure
2
4.2. Rubin Manouver •
vaginal approach •
adduction anterior shoulder by pressing the posterior shoulder towards the chest
• Consider episiotomy
Rubin 1964 recommended two maneuvers. First, the fetal shoulders are rocked from side to side by applying force to the maternal abdomen. If this is not successful,
the pelvic hand reaches the most easily accessible fetal shoulder, which is then pushed toward the anterior surface of the chest. This maneuver most often abducts
both shoulders, which in turn produces a smaller shoulder-to-shoulder diameter. This permits displacement of the anterior shoulder from behind the symphysis.
4
Medical Education Unit Faculty of Medicine Udayana University
59
a b
Figure 10.6. Rubin Manouver. A. The shoulder-to-shoulder diameter is aligned vertically. B. The more easily accessible fetal shoulder the anterior is shown here is
pushed toward the anterior chest wall of the fetus arrow. Most often, this results in abduction of both shoulders, which reduces the shoulder-to-shoulder diameter and frees
the impacted anterior shoulder
1
5. Rotate the posterior shoulder- Corkscrew Wood Maneuver
Woods 1943 reported that by progressively rotating the posterior shoulder 180 degrees in a corkscrew fashion, the impacted anterior shoulder could be released. This is
frequently referred to as the Woods corkscrew maneuver.
4
Figure 10.7. Wood Maneuver. The hand is placed behind the posterior shoulder of the fetus. The shoulder is then rotated progressively 180 degrees in a corkscrew manner so
that the impacted anterior shoulder is released
1
6. Manual removal of posterior arm
