The 17-year-old girl suddenly became unconscious, why?

Hypoglycemia is one of the more common metabolic diseases, but repeated or persistent hypoglycemia can lead to damage to the central nervous system.
In severe cases, it can cause hypoglycemic encephalopathy, leaving short-term and long-term sequelae
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Therefore, early identification of hypoglycemia and its risk factors, timely monitoring, intervention and treatment, to prevent the occurrence of hypoglycemic encephalopathy is particularly important
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Come and learn together through the following cases! Author: Wang Lulu (Hebei Provincial People's Hospital) This article is published with the authorization of the author, and please do not reprint without authorization
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Female, 17 years old, patient with unconsciousness for 3 hours, female, 17 years old
.

3 hours before admission to the hospital, he was found unconscious by his family, and he did not respond to calls or wake up.
The CT scan showed no abnormality in the local hospital, and he came to the emergency department of our hospital for further diagnosis and treatment
.

The patient's recent diet and sleep were normal, and there was no abnormality in the second stool, and there was no significant change in body weight
.

A history of upper respiratory tract infection 8 days ago, manifested as cough, hoarseness, and no fever.
The symptoms improved after taking "cold medicine (the name and dosage of the medicine is unknown)" by himself
.

Denied the history of hypertension, diabetes, etc.
, and denied the history of infectious diseases
.

The mother is diabetic and the father is healthy
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➤Physical examination T37.
9℃, R17 times/min, P85 times/min, BP104/71mmHg, coma, double pupils are large and equal round, sensitive to light reflex, eyeballs in both eyes are centered, intermittently visible eyeball floating, bilateral forehead lines and nose The labial sulcus was symmetrical, with occasional right limb movement under orbital pressure stimulation, but no movement of the left limb, slightly low limb muscle tone, normal tendon reflexes on both sides, negative Babinski sign on both sides, and positive Chaddock on both sides
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Kernig's sign was positive
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The rest of the nervous system examination could not cooperate
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Glasgow score (disorder of consciousness score): 6 points (eye opening: 1 point; language: 1 point; exercise: 4 points) ➤Auxiliary examination blood gas analysis: PH 7.
46, PaCO2 30.
80mmHg, PaO2 130.
30mmHg, SaO2 98.
5%, blood glucose 4.
01 mmol/L
.

Blood routine analysis: WBC22.
16×109/L; NET87.
30%
;
 Rapid D-dimer, four coagulation items, all emergency items, and blood ammonia were generally normal
.

Head CT: The density of the right cerebral hemisphere is lower than that of the contralateral side, the boundary between gray and white matter is not clear, the multiple sulci have become shallow and disappeared, and the brain tissue is swollen.
Considering the possibility of cerebral infarction, MRI is recommended
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Cranial MRI+MRA+DWI+SWI: The right frontotemporal parietal occipital lobe and corpus callosum spresso are more likely to have acute cerebral infarction
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The right middle cerebral artery blood flow signal was under-rimmed, and endarteritis was not excluded
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 Head CT, head MRI + MRA + DWI + SWI ➤ Qualitative analysis of the patient's coma, considering the damage to the cerebral cortex and the reticular ascending activation system; the patient's bilateral Chaddock was positive, and the right limb was occasionally moved by orbital pressure stimulation, and the left limb was not.
See activity, consider bilateral pyramidal tract damage, and the right side is predominant; the patient's Kernig sign is positive, and meningeal irritation sign is considered
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According to the analysis of the above auxiliary examination results, it is considered that the patient's disease is related to the central nervous system infection, but at this moment, the patient's fingertip blood sugar is routinely checked, and the random blood sugar: 0.
03mmol/L! ! ! Retest random blood sugar: 1.
6mmol/L
.

Further inquiries about the medical history revealed clues: the patient is usually cautious, and he likes to dig into the horns, and he had a quarrel with his mother two days ago; the mother has diabetes, and there are antidiabetic drugs such as metformin, glyburide, and insulin at home.

.

Therefore, we performed a toxicological analysis
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Toxicological analysis: metformin drug concentration 25.
4mg/L (therapeutic dose <15mg/L)
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Therefore, it is considered that the patient has severe brain dysfunction due to excessive intake of hypoglycemic drugs resulting in hypoglycemia
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Therefore, a preliminary diagnosis of hypoglycemic encephalopathy was made
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The patients were given sugar supplements to correct hypoglycemia, mannitol to reduce intracranial pressure, and nutritional support and other symptomatic treatments, and the patient's consciousness gradually recovered
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Discussion ➤ Why was the patient normoglycemic in the emergency department? The patient's blood glucose was 4.
01 mmol/L at the time of consultation, which was within the physiological range, and the blood glucose was re-monitored after hospitalization to 0.
03 mmol/L
.

This may be caused by stress, which can lead to increases in epinephrine and glucagon, promoting hepatic glycogenolysis, and responsively increasing blood glucose levels
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Therefore, for comatose patients, blood glucose should be measured repeatedly to avoid delay in the diagnosis and treatment of hypoglycemic encephalopathy
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➤Etiology and mechanism of hypoglycemic encephalopathy Hypoglycemic encephalopathy is often caused by unreasonable medication, excessive endogenous insulin secretion, sepsis, alcoholism, liver and kidney failure, and unexplained endocrine diseases
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When the patient's blood sugar is lower than 2.
3mmol/L, he can fall into a coma
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A coma for more than 6 hours can cause irreversible damage to nerve cells
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Hypoglycemia promotes energy consumption by nerve cells, leading to loss of membrane ion pump function, resulting in the transfer of water from extracellular to intracellular
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Some studies suggest that the death of hypoglycemic brain neurons is not caused by insufficient energy, but is related to the activation of neuronal nicotinamide adenine dinucleotide phosphate oxidase during glucose reperfusion.

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➤ Imaging examination of hypoglycemic encephalopathy Magnetic resonance imaging (MRI) features are as follows: (1) Involvement is more common in the cerebral cortex, hippocampus, basal ganglia, corpus callosum, and rarely in the cerebellum, brainstem and thalamus
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This is because the activity of the latter glucose transporter is higher, as is the level of adenosine triphosphate in the thalamus
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(2) MRI showed high signal on DWI and FLAIR, mild high signal on T2WI, and mild low signal on T1WI
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DWI plays an important role in the early diagnosis of hypoglycemic encephalopathy
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(3) Brain imaging of hypoglycemic encephalopathy is not always diffuse or bilateral
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Probably due to the metabolic asymmetry between the left and right hemispheres, the glucose metabolism in the left hemisphere is lower than that in the right hemisphere
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Therefore, the right side of the brain is more likely to be affected
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(4) Hypoglycemia can also cause cerebrovascular disease, swelling of capillary endothelial cells, narrowing of capillary lumen, and circulatory disturbance
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➤Treatment of hypoglycemic encephalopathy At present, for patients with hypoglycemic encephalopathy, intravenous infusion of glucose should be given immediately to correct hypoglycemia quickly and effectively
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Monitor your blood sugar repeatedly to keep your blood sugar within the normal range
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Summary Hypoglycemic encephalopathy often involves the cerebral cortex, basal ganglia, and corpus callosum
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In clinical practice, the possibility of hypoglycemic encephalopathy should be considered if lesions occur in the above-mentioned regions and do not conform to a specific cerebral arterial distribution
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In elderly patients, hypoglycemic encephalopathy is often caused by overuse of hypoglycemic drugs
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However, in adolescents, due to various psychological problems, the possibility of suicide by drug or poison should be considered, and the patient should be asked in detail about his personality, whether he had mood swings before the onset of the disease, whether he had a history of exposure to drugs or drugs, and whether he had been exposed to drugs or drugs.
Those who provide detailed information should be screened for toxicology as early as possible to avoid delays in diagnosis and treatment
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In addition, one should be alert to transient "normalization" of blood glucose and monitor blood glucose repeatedly
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References: 1.
Ma JH, Kim YJ, Yoo WJ, Ihn YK, Kim JY, Song HH, et al.
MR imaging of hypoglycemic encephalopathy: lesion distribution and prognosis prediction by diffusion-weighted imaging.
Neuroradiology 2009;51:641– 649.
doi: 10.
1007/s00234-009-0544-5.
2.
Barbara G, Mégarbane B, Argaud L, Louis G, Lerolle N, Schneider F, et al.
Functional outcome of patients with prolonged hypoglycemic encephalopathy.
Ann Intensive Care 2017;7 :54.
doi: 10.
1186/s13613-017-0277-2.
3.
Aoki T, Sato T, Hasegawa K, Ishizaki R, Saiki M.
Reversible hyperintensity lesion on diffusion-weighted MRI in hypoglycemic coma.
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4.
Suh SW, Gum ET, Hamby AM, Chan PH, Swanson RA.
Hypoglyce-mic neuronal death is triggered by glucose reperfusion and activation of neuronal NADPH oxidase.
J Clin Invest 2007; 117:910–918.
doi: 10.
1172/JCI30077.