Hypoglycemic shock is characterized as the body joss of fluids, such cases are hemorrhage due to trauma, dehydration as a result of vomiting and severe diarrhea or from severe burns (Hand 2001). According to Killeen (2007), there are four stages of shock : initial, compensatory, progressive and refractory. In the initial stage signs of shock are minimal with cells switching from aerobic to anaerobic metabolism leading to lactic acidosis, this is the build-up of excess lactic acid in the blood. Taking an arterial blood gas and checking the lactate level in the blood can give clear indication of acidosis.
Hypoglycemia can manifest when there is bout 15% loss of circulatory volume, but the more volume lost the more significant the clinical signs become (Hall, 2010). The next stage of shock is the compensatory stage, here the body is attempting to stabilize the body circulation. This is where body compensatory mechanisms fall in to play; the initial compensatory mechanism is the sympathetic nervous response. Here the response is mediated by the decrease in arterial pressure which then stimulates the preceptors located in the aortic arch and carotid sinuses (Marine 1998).
The result of the nervous system being stimulated is the lease of catecholamine, noradrenalin and adrenaline (Shaver and Brewer 2002). An effect of adrenaline release is it stimulates the beta receptors in the heart increasing myocardial contractile and vasoconstriction thus improving cardiac output and increasing the blood pressure. This neurological reaction causes the body to shift blood from the Nan-vital organs such as the skin to the more vital organs like the heart and lungs resulting in hypertrophied organs and tissues. The rennin-negotiations- lodestone (RASA) mechanism is stimulated when there is a decrease in dined perfusion.
Rennin is released by the kidneys and converted in the blood through the ingeniousness’s to negotiations 1 . Then from the lungs negotiations 1 is converted into negotiations 2. Negotiations 2 has two important roles the release of noradrenalin causing vasoconstriction and the release of lodestone. Vasoconstriction maintains blood pressure while there is acute blood loss, and lodestone causes an increase of sodium reapportion in an attempt to conserve water and maintain intramuscular volume. The end result is reduced urine output of less than mils ‘her. At this
Stage clinical signs that can be seen are increased heartbeat as there is increased cardiac contractile and increase in glucose levels as a result of adrenaline release. In addition tachycardia, increase in temperature, pale cool skin as blood is shifted away from the skin. F-rather symptoms seen in patients are a change in mental state, increased respiratory rate absent bowel sounds and complaining of thirst (Killeen 2007), These compensatory mechanisms will eventually stop working if the source of the problem is not rapidly treated in this case hemorrhage.
As more blood is lost there is a crease in perfusion causing electrolyte imbalance and metabolic and respiratory acidosis. At this refractory stage prognosis is uncertain. If these clinical signs are left untreated for long enough the shock will enter its final and irreversible stage known as refractory in which death is likely (Hand 2001). The initial assessment can be done by the bedside by offering a hand shake and asking the patient a simple question. Listening to them is important because you make sense of their mental state. This assessment can tell the nurse the individual’s conscious level, main. Ay potency, and Raphael perfusion. This also makes the patient feels safe as they are able to trust the nurse and are less likely to be anxious and distressed. It is also beneficial to find out any past and recent relevant medical history. Ata glance the patient’s skin shows a pale color, there is evidence Of trauma as there is blood loss, they are restless and anxious but conscious. As the patient is showing signs of shock being present they require an immediate SABA to be done. The airway needs to be assessed; a sign of partial obstruction can be gurgling or snoring sounds when they breathe.
One common cause of airway obstruction is when the individual loses consciousness. What happens is they are unable to maintain their own away and their tongue usually falls back causing the obstruction. To quickly assess their airway the PAPUA (alert, responds to voice, responds to pain or unresponsive) method can be used. If the patient is able to speak it is an indication that their airway is clear. However if the patient is unconscious an orphanages or encephalopathy may be used to maintain a patent airway by preventing their tongue falling back (Alert ,2012).
The next stage is to assess their breathing measuring respiratory rate the tenant in this case is presenting with tachyon and is unable to complete sentences, they are using their accessory muscles and presenting with cannabis. They are tachycardia, hypertensive and oxygen saturation is reduced. The patient should receive high flow oxygen have IV access secured and continuous BP, oxygen saturation and EGG monitoring. The oxygen therapy efficacy should be monitored using pulse geometry and aim for saturation between 94% – 98%.
The optimal oxygen delivery is using a non- reverberate mask; the reservoir bag is inflated at a rate of 1 51 per min, this ask delivers 60% to 85% 02 (Resuscitation Council UK, 2005). Following breathing stage, the circulatory assessment can begin, in patients with hypoglycemic there is confusion, cold extremities, tachycardia, hypertension, Algeria and reduced capillary refill. Immediately attempts to resuscitate the shocked patient must begin, as well as gaining venous access as there is the risk of peripheral shutdown.
Administer IV fluids as per NICE IV Fluid therapy guidelines 2013. Fifth patient is conscious the nurse should take this opportunity to question them about previous incidents of bleeding ND any relevant past medical history. A blood sample should be obtained to be taken for cross-matching for blood transfusion as the patient will require blood transfusion. The nurse should check the patient wrist band before administering any drug. With blood transfusion they need to get another nurse to check with before administering.
Also other ways that can determine the severity of patient’s condition are testing the hemoglobin levels, urea and electrolytes and a liver function test. Initially the main priority is to stop any bleeding. An indication that the patient s in hypoglycemic shock is their pulse being above BPML and a systolic blood pressure less than might, thus requiring intravenous infusion. Already intravenous access would have been obtained. The lost fluids are usually replaced with crystallites this would be normal saline, and should be warm to prevent hypothermia.
Other nursing interventions at this point would be to monitor urine output through a catheter. To successfully manage the GIG bleed surgical intervention is needed, but before this the exact location of the bleed must be confirmed, an endoscope would be a way of achieving this. Next is the disability assessment which refers to the neurological state of the patient, this includes assessing their conscious level. Measuring their motor power, normal power will show no weakness when given a command such as squeeze my hand or bend your knees. A pupil gauge should be used to check whether both eyes are equal and reactive to light.
Again to rapidly assess their level of consciousness the PAPUA score is a recommended technique. If a patient is not responding to vocal stimuli then a method to induce pain may be done such as pressing into the bed of their finger nail. Finally the last assessment is a complete examination from head to toe; this includes looking at their skin condition, and any signs of injury or trauma. The nurse should also re-position the patient to regularly to check pressure areas; similarly the patient should be nursed on a pressure relieving mattress as they are not very mobile.
Additionally, take into consideration any environmental factors that affect the patient’s core temperature, for example if a window is left open. At this point the patient would be in no immediate clinical danger and tests can be ordered to make clear diagnosis. For example an MR. scan or an endoscope. Following the bedside A-E assessment it is highly likely that the nurse will need to discuss further management of the shocked patient with colleagues to ensure the patient is in the right unit for their level of care, so if needed to be transferred to HEAD, or TIT for close observation.
The NASH Institute for Innovation and Improvement, 2006 has recommended the use of situation, background, assessment and recommendation (SABA). To conclude, shock is a critical condition where there is inadequate tissue perfusion as a result of fluid or blood loss. Nurses need to recognize the clinical signs of this shock to be able to reverse it before organ damage occurs which is irreversible. The following nursing interventions are crucial in managing the shocked patient and enhancing their recovery process.
To ensure a patent airway and sufficient circulation, provide I. V. Infusion with normal saline given through a large bore. Take arterial blood sample which measures blood gases and monitor these frequently as directed. Ensure an indwelling urinary catheter is inserted and measure urine output hourly. Preferably attach them to a cardiac monitor and record the patients expiratory rate, pulse, blood pressure, oxygen saturation and temperature regularly.